Neuroinflammation and oxidative stress act in concert to promote neurodegeneration in the diabetic retina and optic nerve:galectin-3 participation

Diabetes is a lifelong disease characterized by glucose metabolic imbalance,in which low insulin levels or impaired insulin signaling lead to hyperglycemic state.Within 20 years of diabetes progression,95%of patients will have diabetic retinopathy,the leading cause of visual defects in working-age people worldwide.Although diabetes is considered a microvascular disease,recent studies have shown that neurodegeneration precedes vascular changes within the diabetic visual system,albeit its mechanisms are still under investigation.Neuroinflammation and oxidative stress are intrinsically related phenomena,since macrophage/microglia and astrocytes are the main sources of reactive oxygen species during central nervous system chronic degenerative diseases,and both pathological processes are increased in the visual system during diabetes.The present review will focus on recent findings of the contribution of oxidative stress derived from neuroinflammation in the early neurodegenerative aspects of the diabetic visual system and their relationship with galectin-3.

Influence ofα-Lipoic acid adjuvant therapy on sugar metabolism,peripheral nerve conduction velocity and oxidative stress in patients with diabetic peripheral neuropathy

Objective: To explore the influence of α-Lipoic acid adjuvant therapy on glucose metabolism, peripheral nerve conduction velocity and oxidative stress in patients with diabetic peripheral neuropathy. Methods: A total of 92 cases of patients with diabetic peripheral neuropathy were divided into observation group and control group according to the odd and even admission number, 46 cases in each group. All patients were given the conventional treatment, on this basis, patients in control group were given orally Pancreatic Kinionoge, patients in observation group were given α-Lipoic acid intravenous injection. They were treated for 14 d. The following indicators were observed in two groups before and after treatment: glucose metabolic index: fasting blood glucose (FBG), 2 h postprandial blood glucose (2hPBG) and glycosylated hemoglobin (HbA1c);peripheral nerve conduction velocity, median nerve, sensory nerve conduction velocity of nervus peroneus communis (MCV) and motor nerve conduction velocity (SCV), ankle arm index (ABI) and inner diameter of lower limb artery (femoral artery, dorsalis pedis artery, popliteal artery), oxidative stress indicators: superoxide dismutase (SOD) and malondialdehyde (MDA). Results: Compared with before treatment, the FBG, 2hPBG, HbA1c level in two groups after treatment were significantly reduced, but the difference of intergroup after treatment was no statistical significance;MCV and SCV of median nerve and nervus peroneus communis was increased significantly than control group after treatment, moreover MCV and SCV of median nerve and nervus peroneus communis in observation group were higher than control group after treatment, the difference was significant. After treatment, ABI and femoral artery, dorsalis pedis arteries, popliteal artery inner diameter in two groups were increased significantly, moreover after treatment the above level in observation group was obviously higher than control group, there was significant difference. After treatment, the MDA in observation group were reduced significantly and SOD level increased significantly, difference was statistically significant compared with before treatment and control group after the treatment;The difference in control group compared between before treatment and after treatment had no statistical significance. Conclusion: Diabetic peripheral neuropathy treated adjuvantly by α-Lipoic acid can significantly improve lower limb blood supply, improve the peripheral nerve conduction velocity, reduce level of oxidative stress, the effect on glucose metabolism still need long course of observation.

Correlation of serum uric acid level with neurotrophy, nerve injury and systemic oxidative stress response in patients with Parkinson's disease

Objective:To investigate the correlation of serum uric acid level with neurotrophy, nerve injury and systemic oxidative stress response in patients with Parkinson's disease.Methods:A total of 60 patients with Parkinson's disease who were diagnosed and treated in our hospital between July 2014 and February 2018 were enrolled in Parkinson's disease group, and 100 healthy elderly people who received physical examination in our hospital during the same period were enrolled in normal control group. The differences in serum uric acid levels as well as the contents of indexes related to neurotrophy, nerve injury and oxidative stress were compared between the two groups, and Pearson test was used to evaluate the correlation of serum uric acid level with indexes related to neurotrophy, nerve injury and oxidative stress in patients with Parkinson's disease.Results:Serum uric acid level of PD group was lower than that of normal control group;serum neurotrophy indexes BDNF, GDNF and NGF contents were lower than those of normal control group;serum nerve injury indexes YKL-40 and S-100B contents were higher than those of normal control group whereas IGF-1 content was lower than that of normal control group;serum oxidative stress indexes GPX and CAT contents were lower than those of normal control group whereas MDA and LHP contents were higher than those of normal control group. Correlation analysis confirmed that the serum uric acid level of patients with Parkinson's disease was directly correlated to the indexes related to neurotrophy, nerve injury and oxidative stress.Conclusion:The abnormal decrease of serum uric acid level in patients with Parkinson's disease is directly correlated with the neurotrophy, nerve injury, oxidative stress response, and so on.

Effects of mild hypothermia irrigation fluid on nerve function and oxidative stress during intracranial hematoma irrigation

Objective: To study the effects of mild hypothermia irrigation fluid on nerve function and oxidative stress during intracranial hematoma irrigation. Methods: The patients with hypertensive cerebral hemorrhage who received hematoma aspiration in our hospital between August 2014 and November 2017 were chosen and randomly divided into the observation group who received mild hypothermia irrigation fluid and the control group who received room temperature irrigation fluid. Before treatment and 72 h after treatment, the contents of nerve injury markers, cytokines and oxidative stress mediators were measured after peripheral blood extraction and serum separation. Results: Compared with those of control group, serum neuron-specific enolase (NSE), visinin-like protein-1 (VILIP-1), glial fibrillary acidic protein (GFAP), neuropeptide Y (NPY), platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF), high mobility group protein B1 (HMGB1), macrophage migration inhibitory factor (MIF), interleukin-1β (IL-1β), interleukin-10 (IL-10), malondialdehyde (MDA), 8-OHdG and nitric oxide (NO) contents of observation group were significantly lower whereas serum brain-derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1) and total antioxidant capacity (TAOC) contents were significantly higher after treatment (P<0.05). Conclusion: The application of mild hypothermia irrigation fluid during intracranial hematoma irrigation can alleviate the nerve function injury, improve the neurotrophic status and inhibit the oxidative stress response.

Effects of gangliosides combined with family rehabilitation training on nerve injury, neurodevelopment and oxidative stress in children with HIE

Objective:To study the effects of gangliosides combined with family rehabilitation training on nerve injury, neurodevelopment and oxidative stress in children with HIE.Methods:Children with HIE who were treated in Zigong Third People's Hospital between March 2015 and October 2017 were selected and randomly divided into two groups, rehabilitation training group received gangliosides combined with family rehabilitation training and negative control group accepted gangliosides combined with conventional rehabilitation intervention. The contents of nerve injury molecules, neurotrophic molecules and oxidative stress molecules in serum were measured before intervention and 3 months after intervention.Results: Compared with those of same group before intervention, serum VILIP1, NSE, UCH-L1, TNF-α, IL-6, NO, DM and MDA levels of both groups of children were significantly lower whereas BDNF, TRKB, NTF, NGF, SOD and GSH-PX levels were significantly higher 3 months after intervention, and serum VILIP1, NSE, UCH-L1, TNF-α, IL-6, NO, DM and MDA levels of rehabilitation training group after intervention were lower than those of negative control group whereas BDNF, TRKB, NTF, NGF, SOD and GSH-PX levels were higher than those of negative control group.Conclusion: Gangliosides combined with family rehabilitation training can reduce the nerve injury, improve the neurodevelopment and inhibit the oxidative stress in children with HIE.

Effect of acupuncture combined with drug therapy on the nerve cytokine secretion and oxidative stress in convalescence of cerebral infarction

Objective: To explore the effect of acupuncture combined with drug therapy on the nerve cytokine secretion and oxidative stress in convalescence of cerebral infarction. Methods: A total of 118 patients in convalescence of cerebral infarction who were treated in the affiliated hospital of our school between August 2014 and December 2016 were divided into control group (n=59) and observation group (n=59) according to the random number table method. Control group received routine drug therapy, and the observation group received acupuncture combined with drug therapy. The differences in serum levels of neurotrophic factors, nerve injury factors and oxidative stress indexes were compared between the two groups before and after treatment. Results: The differences in serum levels of neurotrophic factors, nerve injury factors and oxidative stress indexes were not statistically significant between the two groups before treatment. After treatment, serum neurotrophic factors IGF-1, BDNF and NGF levels of observation group were higher than those of control group;nerve injury factors S-100β, NSE, GFAP and UCH-L1 levels were lower than those of control group;oxidative stress indexes MDA, AOPPs and LHP levels were lower than those of control group while SOD and GSH-Px levels were higher than those of control group. Conclusion: Acupuncture combined with drug therapy can effectively optimize the nerve function, reduce the nerve injury and suppress the systemic oxidative stress response of patients in convalescence of cerebral infarction.

Effect of rehabilitation training combined with hyperbaric oxygen therapy on the nerve cytokine secretion and oxidative stress in rehabilitation period of patients with cerebral infarction

Objective: To discuss the influence of rehabilitation training combined with hyperbaric oxygen therapy on the nerve cytokine secretion and oxidative stress in rehabilitation period of patients with cerebral infarction. Methods: A total of 110 patients with cerebral infarction who received rehabilitation therapy in the hospital between January 2015 and May 2017 were divided into routine group (n=55) and hyperbaric oxygen group (n=55) according to random number table. Routine group received regular rehabilitation training, and hyperbaric oxygen group underwent rehabilitation training combined with hyperbaric oxygen therapy. The differences in the serum contents of nerve factors, neurotransmitters and oxidative stress indexes were compared between the two groups at immediately after admission (T0) and after 14 d of treatment (T1). Results: At T0, there was no statistically significant difference in the serum contents of nerve factors, neurotransmitters and oxidative stress indexes between the two groups. At T1, serum nerve factors MBP and NSE contents of hyperbaric oxygen group were lower than those of routine group while NGF content was higher than that of routine group;serum neurotransmitter Glu content was lower than that of routine group while GABA content was higher than that of routine group;serum oxidative stress indexes ROS and LHP contents were lower than those of routine group while CAT and SOD contents were higher than those of routine group. Conclusion: Rehabilitation training combined with hyperbaric oxygen therapy can effectively optimize the nerve function and inhibit the systemic oxidative stress response in rehabilitation period of patients with cerebral infarction.

Effect of α-lipoic acid combined with nerve growth factor on bone metabolism, oxidative stress and nerve conduction function after femoral fracture surgery

Objective: To discuss the effect of α-lipoic acid combined with nerve growth factor on bone metabolism, oxidative stress and nerve conduction function after femoral fracture surgery. Methods: A total of 110 patients with femoral fracture who received surgical treatment in the hospital between January 2015 and January 2017 were collected and divided into the control group (n=55) and study group (n=55) by random number table. Control group received postoperative nerve growth factor therapy, and study group received postoperative α-lipoic acid combined with nerve growth factor therapy. The differences in the contents of bone metabolism and oxidative stress indexes as well as the levels of nerve conduction function indexes were compared between the two groups before and after treatment. Results: Before treatment, the differences in the contents of bone metabolism and oxidative stress indexes as well as the levels of nerve conduction function indexes were not statistically significant between the two groups. After treatment, serum bone metabolism indexes BGP and PⅠNP contents of study group were higher than those of control group while CTX-Ⅰ and TRAP contents were lower than those of control group;serum oxidative stress indexes TAC, CAT and SOD contents of study group were higher than those of control group while MDA content was lower than that of control group;limb nerve conduction velocity SCV and MCV levels of study group were higher than those of control group. Conclusion: α-lipoic acid combined with nerve growth factor therapy after femoral fracture surgery can effectively balance osteoblast/osteoclast activity, reduce oxidative stress and improve limb nerve conduction velocity.

Effect of early enteral nutrition intervention on nerve function, systemic oxidative stress and inflammatory response in patients with hypertensive cerebral hemorrhage

Objective: To study the effect of early enteral nutrition intervention on nerve function, systemic oxidative stress and inflammatory response in patients with hypertensive cerebral hemorrhage. Methods: A total of 98 patients with hypertensive cerebral hemorrhage who received hospitalization in the hospital between April 2015 and February 2017 were collected and divided into control group and observation group by random number table method, 49 cases in each group. Control group received routine enteral nutrition intervention and observation group received early enteral nutrition intervention. The differences in serum levels of nerve function-related indexes, oxidative stress indexes and inflammatory mediators were compared between the two groups of patients before and after intervention. Results: Before intervention, the differences in serum levels of nerve function-related indexes, oxidative stress indexes and inflammatory mediators were not statistically significant between the two groups of patients. After 1 week of intervention, serum S100B, NSE, GFAP, MBP, LPO, MDA, PCT, IL-1β, IL-6 and TNF-α levels of both groups of patients were lower than those before intervention while GSH-PX levels were higher than those before intervention, and serum S100B, NSE, GFAP, MBP, LPO, MDA, PCT, IL-1β, IL-6 and TNF-α levels of observation group were lower than those of control group while GSH-PX level was higher than that of control group. Conclusion:Early enteral nutrition intervention can effectively optimize the nerve function and suppress the systemic oxidative stress and inflammatory response in patients with hypertensive cerebral hemorrhage.

The effects of large doses of vitamin C and vitamin E on nerve injury, neurotrophic and oxidative stress in patients with acute craniocerebral injury

Objective:To study the effects of large doses of vitamin C and vitamin E on nerve injury,neurotrophic and oxidative stress in patients with acute craniocercbral injury.Methods:Patients with acute cranioccrebral trauma who were admitted to the Third People's Hospital of Zigong from April 2014 to December 2016 were selected as the subjects and were randomly divided into two groups.The control group received conventional treatment,and the intervention group received large doses of vitamin C and vitamin E combined with conventional treatment.On the yh day and 7th day after treatment,peripheral blood was collected and serum was isolated,then the contents of nerve injury index NSE,S 100B,NGB,UCH-L1,Tf,Ft and neurotrophic indexes NTF-α,BDNE NGF and IGF-I were determined by Enzyme-linked immunosorbent assay kit,and the contents of SOD,GPx,CAT,OH-,O2,MDA and AOPP were measured by radioactive immunoprecipitation kit.Results:3th day and 7th day after treatment,the contents of NSE,S100B,NGB,UCH-L1,Tf,Ft,NTF-α,BDNF,NGF,IGF-Ⅰ,OH-,O2-,MDA and AOPP in the intervention group were all significantly lower than those in the control group.The content of SOD,GPx and CAT in serum in the intervention group was significantly higher than that in the control group.Conclusions:High-dose vitamin C and vitamin E treatment can alleviate nerve injury,oxidative stress response,and improve neurotrophic state in patients with acute craniocerebral injury.

cAMP/PKA pathway and mitochondrial protection in oxidative stress-induced optic nerve head astrocytes

Oxidative stress and cyclic adenosine 3′,5′-monophosphate(cAMP)/protein kinase A(PKA)pathway in the optic nerve head astrocytes:Glaucoma is a leading cause of blindness worldwide in individuals 60 years of age and older.Despite the widely appreciated disease relevance of structural and functional abnormalities of astrocyte in the optic nerve head(ONH)that is associated with retinal ganglion cell(RGC)axon degeneration,the molecular mechanisms underlying astrocyte dysfunction in glaucomatous ONH degeneration are poorly understood.Oxidative stress is strongly linked to glaucoma pathogenesis,and astrocytes are the responsible cell type that is mostly related to oxidative stress and glaucomatous ONH degeneration.

Acquired sensorineural hearing loss,oxidative stress,and microRNAs

Hearing loss is the third leading cause of human disability.Age-related hearing loss,one type of acquired sensorineural hearing loss,is largely responsible for this escalating global health burden.Noise-induced,ototoxic,and idiopathic sudden sensorineural are other less common types of acquired hearing loss.The etiology of these conditions is complex and multi-fa ctorial involving an interplay of genetic and environmental factors.Oxidative stress has recently been proposed as a likely linking cause in most types of acquired sensorineural hearing loss.Short non-coding RNA sequences known as microRNAs(miRNAs)have increasingly been shown to play a role in cellular hypoxia and oxidative stress responses including promoting an apoptotic response.Sensory hair cell death is a central histopathological finding in sensorineural hearing loss.As these cells do not regenerate in humans,it underlies the irreversibility of human age-related hearing loss.Ovid EMBASE,Ovid MEDLINE,Web of Science Core Collection,and ClinicalTrials.gov databases over the period August 1,2018 to July 31,2023 were searched with"hearing loss,""hypoxamiRs,""hypoxia,""microRNAs,""ischemia,"and"oxidative stress"text words for English language primary study publications or registered clinical trials.Registe red clinical trials known to the senior author we re also assessed.A total of 222studies were thus identified.After excluding duplicates,editorials,retra ctions,secondary research studies,and non-English language articles,39 primary studies and clinical trials underwent full-text screening.This resulted in 11 animal,in vitro,and/or human subject journal articles and 8 registered clinical trial database entries which form the basis of this narrative review.MiRNAs miR-34a and miR-29b levels increase with age in mice.These miRNAs were demonstrated in human neuroblastoma and murine cochlear cell lines to target Sirtuin 1/peroxisome proliferato r-activated receptor gamma coactivator-1-alpha(SIRT1/P GC-1α),SIRT1p53,and SIRT1/hypoxia-inducible factor 1-alpha signaling pathways resulting in increased apoptosis.Furthermore,hypoxia and oxidative stress had a similar adve rse apoptotic effect,which was inhibited by resve ratrol and a myocardial inhibitorassociated transcript,a miR-29b competing endogenous mRNA.Gentamicin reduced miR-182-5p levels and increased cochlear oxidative stress and cell death in mice-an effect that was corrected by inner ear stem cell-derived exosomes.There is ongoing work seeking to determine if these findings can be effectively translated to humans.

Effects of postoperative dexmedetomidine sedation on nerve function, inflammation and oxidative stress in patients with craniocerebral injury

Objective:To study the effects of postoperative dexmedetomidine sedation on nerve function, inflammation and oxidative stress in patients with craniocerebral injury.Methods: Patients who were admitted to ICU and needed sedation and analgesia after craniocerebral injury craniotomy in Huiya Hospital between June 2016 and October 2017 were selected as the research subjects and divided into the Dex group who accepted postoperative dexmedetomidine sedation and the control group who accepted postoperative midazolam sedation according to the history data. The levels of nerve markers and inflammation molecules in serum as well as the expression of oxidative stress molecules in peripheral blood were measured before surgery as well as 24 h and 48 h after surgery.Results: Compared with those before surgery, UCH-L1, NSE, GFAP, sFkn, CXCL12, IL-1β and sICAM1 levels in serum as well as Nrf2, NQO1, HO1, NOX2 and NOX4 expression in peripheral blood of both groups decreased significantly whereas BDNF and NGF levels increased significantly 24 h and 48 h after surgery, and UCH-L1, NSE, GFAP, sFkn, CXCL12, IL-1β and sICAM1 levels in serum as well as Nrf2, NQO1, HO1, NOX2 and NOX4 expression in peripheral blood of Dex group 24 h and 48 h after surgery were significantly lower than those of control group whereas BDNF and NGF levels were significantly higher than those of control group.Conclusion: Dexmedetomidine for postoperative sedation can be more effective than midazolam to improve the nerve function, and reduce the inflammation and oxidative stress in patients with craniocerebral injury.

Hydrogen sulfide reduces oxidative stress in Huntington's disease via Nrf2

The pathophysiology of Huntington's disease involves high levels of the neurotoxin quinolinic acid. Quinolinic acid accumulation results in oxidative stress, which leads to neurotoxicity. However, the molecular and cellular mechanisms by which quinolinic acid contributes to Huntington's disease pathology remain unknown. In this study, we established in vitro and in vivo models of Huntington's disease by administering quinolinic acid to the PC12 neuronal cell line and the striatum of mice, respectively. We observed a decrease in the levels of hydrogen sulfide in both PC12 cells and mouse serum, which was accompanied by down-regulation of cystathionine β-synthase, an enzyme responsible for hydrogen sulfide production. However, treatment with NaHS(a hydrogen sulfide donor) increased hydrogen sulfide levels in the neurons and in mouse serum, as well as cystathionine β-synthase expression in the neurons and the mouse striatum, while also improving oxidative imbalance and mitochondrial dysfunction in PC12 cells and the mouse striatum. These beneficial effects correlated with upregulation of nuclear factor erythroid 2-related factor 2 expression. Finally, treatment with the nuclear factor erythroid 2-related factor 2inhibitor ML385 reversed the beneficial impact of exogenous hydrogen sulfide on quinolinic acid-induced oxidative stress. Taken together, our findings show that hydrogen sulfide reduces oxidative stress in Huntington's disease by activating nuclear factor erythroid 2-related factor 2,suggesting that hydrogen sulfide is a novel neuroprotective drug candidate for treating patients with Huntington's disease.

Effects of Xueshuantong combined with antioxidant drugs on nerve conduction function and oxidative stress in patients with diabetic peripheral neuropathy

Objective:To study the effect of Xueshuantong combined with antioxidant drugs on nerve conduction function and oxidative stress in patients with diabetic peripheral neuropathy. Methods: 138 cases of patients with diabetic peripheral neuropathy who were treated in endocrinology department of our hospital between June 2014 and October 2016 were enrolled and randomly divided into two groups. The combination group received Xueshuantong combined with antioxidant drug therapy, and the control group received antioxidant drug therapy. Before and after treatment, the nerve conduction velocity as well as serum content of oxidative stress indexes and nerve cytokines was measured.Results: 4 weeks and 8 weeks after treatment, common peroneal nerve and median nerve MNCV and SNCV as well as serum SOD, GSH-Px, HO-1, CAT, CNTF, BDNF and SDF-1 levels of both groups were significantly higher than those before treatment while serum MDA, AOPP and 8-OHdG levels were significantly lower than those before treatment, and common peroneal nerve and median nerve MNCV and SNCV as well as serum SOD, GSH-Px, HO-1, CAT, CNTF, BDNF and SDF-1 levels of combination group were significantly higher than those of control group while serum MDA, AOPP and 8-OHdG levels were significantly lower than those of control group.Conclusion:Xueshuantong combined with antioxidant drugs can improve the nerve conduction function, inhibit oxidative stress response and improve neurotrophy status in patients with diabetic peripheral neuropathy.

Correlation of serum bilirubin level with nerve defect, oxidative stress and adhesion molecules in patients with cerebral infarction

Objective: To study the correlation of serum bilirubin level with nerve defect, oxidative stress and adhesion molecules in patients with cerebral infarction. Methods: A total of 85 patients who were diagnosed with acute cerebral infarction in Huangshi Central Hospital between August 2014 and March 2017 were selected as the ACI group of the research, and 62 healthy volunteers who received physical examination in Huangshi Central Hospital over the same period were selected as control group. The levels of bilirubin and the contents of nerve defect markers, oxidative stress indexes and adhesion molecules in serum as well as the expression of oxidative stress indexes in peripheral blood were measured. Results: Serum TBIL, IBIL, NSE, sTRAIL, sFas, GFAP, S100B, MDA, AOPP, FKN, sICAM-1, sVCAM-1, ALCAM and PECAM-1 contents as well as peripheral blood Nrf-2 and HO-1 mRNA expression of ACI group were greatly higher than those of control group, serum SOD content was greatly lower than that of control group, and DBIL level was not different from that of control group;serum TBIL and IBIL levels of ACI patients were positively correlated with serum NSE, sTRAIL, sFas, GFAP, S100B, MDA, AOPP, FKN, sICAM-1, sVCAM-1, ALCAM and PECAM-1 contents as well as peripheral blood Nrf-2 and HO-1 mRNA expression, and negatively correlated with serum SOD content. Conclusion: The increase of serum TBIL and IBIL levels in patients with cerebral infarction is related to the degree of nerve defect, the activation of oxidative stress and the increased generation of adhesion molecules.

Effect of PAS triple therapy on nerve injury, oxidative stress and inflammatory response in patients with cerebral infarction

Objective: To study the effect of probucol + aspirin + atorvastatin (PAS) triple therapy on nerve injury, oxidative stress and inflammatory response in patients with cerebral infarction. Methods: Patients with acute cerebral infarction who were treated in Affiliated Hospital of Jianghan University between February 2015 and January 2015 were selected and randomly divided into the PAS group who received probucol + aspirin + atorvastatin triple therapy and the control group who received aspirin + atorvastatin double therapy. The markers of nerve injury, oxidative stress and inflammatory response were determined before treatment and 15 d after treatment. Results: 15 d after treatment, peripheral blood Keap-1 expression and serum GPX1 contents of both groups of patients were significantly higher than those before treatment while peripheral blood Nrf-2 and ARE expression as well as serum S100B, NSE, sTRAIL, FKN, HMGB-1, sICAM-1, Chemerin and 8-iso-PGF2α contents were significantly lower than those before treatment, and peripheral blood Keap-1 expression and serum GPX1 content of PAS group were significantly higher than those of control group while peripheral blood Nrf-2 and ARE expression as well as serum S100B, NSE, sTRAIL, FKN, HMGB-1, sICAM-1, Chemerin and 8-iso-PGF2α contents were significantly lower than those of control group. Conclusion: PAS triple therapy can reduce the nerve injury as well as oxidative stress response and inflammatory response in patients with cerebral infarction.

Effect of rehabilitation training combined with neurotrophic therapy on the nerve cytokine secretion and oxidative stress in rehabilitation period of patients with traumatic brain injury

Objective:To study the effect of rehabilitation training combined with neurotrophic therapy on the nerve cytokine secretion and oxidative stress in rehabilitation period of patients with traumatic brain injury.Methods:A total of 98 patients in rehabilitation period of traumatic brain injury who were treated in our hospital between July 2013 and September 2016 were collected and divided into control group and observation group according to the random number table method, and 49 cases in each group. Control group received regular neurotrophic therapy, and observation group received rehabilitation training combined with neurotrophic therapy. The differences in the contents of nerve cytokines and oxidative stress indexes were compared between the two groups before and after intervention.Results:Before intervention, differences in serum levels of nerve injury indexes, neurotrophy indexes, amino acid neurotransmitters and oxidative stress indexes were not statistically significant between the two groups of patients. After intervention, serum nerve injury indexes MBP, NGB, NSE and S-100B levels as well as excitatory amino acids Glu and Asp levels of observation group were lower than those of control group;neurotrophy indexes BDNF and GDNF levels as well as inhibitory amino acids GABA and Gly levels were higher than those of control group;serum oxidative stress indexes SOD and CAT levels were higher than those of control group;MDA level was lower than that of control group.Conclusions:Rehabilitation training combined with neurotrophic therapy can effectively optimize the nerve function and reduce the systemic oxidative stress state of patients in rehabilitation period of traumatic brain injury.

Correlation of serum Tau and 8-iso-PGF2α levels with nerve injury and oxidative stress in patients with traumatic brain injury

Objective: To study the correlation of serum Tau and 8-iso-PGF2α levels with nerve injury and oxidative stress in patients with traumatic brain injury. Methods: A total of 56 patients who were diagnosed with traumatic brain injury in Pidu District People's Hospital between May 2014 and February 2017 were selected as the TBI group, and 45 volunteers who received physical examination in the hospital during the same period were selected as control group. Serum samples were collected to determine the contents of Tau, 8-iso-PGF2α, nerve cell apoptosis molecules and anti-oxidation molecules. Results: Serum Tau, 8-iso-PGF2α, Bax, Caspase-3 and Caspase-9 levels in TBI group were significantly higher than those in control group while Bcl-2, GSH, VitE, GSH-Px, SOD and HO-1 levels were significantly lower than those in control group;serum Bax, Caspase-3 and Caspase-9 levels in TBI patients with higher Tau level were significantly higher than those in TBI patients with lower Tau level while Bcl-2 level was significantly lower than that in TBI patients with lower Tau level;serum GSH, VitE, GSH-Px, SOD and HO-1 levels in TBI patients with higher 8-iso-PGF2α level were significantly lower than those in TBI patients with lower 8-iso-PGF2α level. Conclusion:Abnormal elevation of Tau and 8-iso-PGF2α levels in serum of patients with traumatic brain injury is related to the excessive apoptosis of nerve cells and the excessive activation of oxidative stress.

Activation of the wnt/β-catenin/CYP1B1 pathway alleviates oxidative stress and protects the blood-brain barrier under cerebral ischemia/reperfusion conditions

Accumulating evidence suggests that oxidative stress and the Wnt/β-catenin pathway participate in stroke-induced disruption of the blood-brain barrier.However,the potential links between them following ischemic stroke remain largely unknown.The present study found that cerebral ischemia leads to oxidative stress and repression of the Wnt/β-catenin pathway.Meanwhile,Wnt/β-catenin pathway activation by the pharmacological inhibito r,TWS119,relieved oxidative stress,increased the levels of cytochrome P4501B1(CYP1B1)and tight junction-associated proteins(zonula occludens-1[ZO-1],occludin and claudin-5),as well as brain microvascular density in cerebral ischemia rats.Moreove r,rat brain microvascular endothelial cells that underwent oxygen glucose deprivation/reoxygenation displayed intense oxidative stress,suppression of the Wnt/β-catenin pathway,aggravated cell apoptosis,downregulated CYP1B1and tight junction protein levels,and inhibited cell prolife ration and migration.Overexpression ofβ-catenin or knockdown ofβ-catenin and CYP1B1 genes in rat brain mic rovascular endothelial cells at least partly ameliorated or exacerbated these effects,respectively.In addition,small interfering RNA-mediatedβ-catenin silencing decreased CYP1B1 expression,whereas CYP1B1 knoc kdown did not change the levels of glycogen synthase kinase 3β,Wnt-3a,andβ-catenin proteins in rat brain microvascular endothelial cells after oxygen glucose deprivatio n/reoxygenation.Thus,the data suggest that CYP1B1 can be regulated by Wnt/β-catenin signaling,and activation of the Wnt/β-catenin/CYP1B1 pathway contributes to alleviation of oxidative stress,increased tight junction levels,and protection of the blood-brain barrier against ischemia/hypoxia-induced injury.