Mufangji tang ameliorates pulmonary arterial hypertension through improving vascular remodeling,inhibiting inflammatory response and oxidative stress,and inducing apoptosis

Background:Mufangji tang(MFJT)is composed of Ramulus Cinnamomi,Radix Ginseng,Cocculus orbiculatus(Linn.)DC.,and Gypsum.In clinical settings,MFJT has been effectively employed in addressing a range of respiratory disorders,notably including pulmonary arterial hypertension(PAH).However,the mechanism of action of MFJT on PAH remains unknown.Methods:In this study,a monocrotaline-induced PAH rat model was established and treated with MFJT.The therapeutic effects of MFJT on PAH rat model were evaluated.Network pharmacology was conducted to screen the possible targets for MFJT on PAH,and the molecular docking between the main active components and the core targets was carried out.The key targets identified from network pharmacology were tested.Results:Results showed significant therapeutic effects of MFJT on PAH rat model.Analysis of network pharmacology revealed several potential targets related to apoptosis,inflammation,oxidative stress,and vascular remodeling.Molecular docking showed that the key components were well docked with the core targets.Further experimental validation results that MFJT treatment induced apoptosis(downregulated Bcl-2 levels and upregulated Bax levels in lung tissue),inhibited inflammatory response and oxdative stress(decreased the levels of IL-1β,TNF-α,inducible NOS,and malondialdehyde,and increased the levels of endothelial nitric oxide synthase,nitric oxide,glutathione and superoxide dismutase),reduced the proliferation of pulmonary arterial smooth muscle cells(downregulated ET-1 andβ-catenin levels and ERK1/2 phosphorylation,increased GSK3βlevels).Conclusion:Our study revealed MFJT treatment could alleviate PAH in rats via induction of apoptosis,inhibition of inflammation and oxidative stress,and the prevention of vascular remodeling.

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.

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.

Antagonistic Effects of N-acetylcysteine on Mitogen-activated Protein Kinase Pathway Activation, Oxidative Stress and Inflammatory Responses in Rats with PM2.5 Induced Lung Injuries

Objective To evaluate the antagonistic effects of N-acetylcysteine(NAC)on mitogen-activated protein kinases(MAPK)pathway activation,oxidative stress and inflammatory responses in rats with lung injury induced by fine particulate matter(PM2.5).Methods Forty eight male Wistar rats were randomly divided into six groups:blank control group(C1),water drip control group(C2),PM2.5 exposed group(P),low-dose NAC treated and PM2.5 exposed group(L),middle-dose NAC treated and PM2.5 exposed group(M),and high-dose NAC treated and PM2.5 exposed group(H).PM2.5 suspension(7.5 mg/kg)was administered tracheally once a week for four times.NAC of 125 mg/kg,250 mg/kg and 500 mg/kg was delivered intragastrically to L,M and H group respectively by gavage(10 ml/kg)for six days before PM2.5 exposure.The histopathological changes and human mucin 5 subtype AC(MUC5AC)content in lung tissue of rats were evaluated.We investigated IL-6 in serum and bronchoalveolar lavage fluid(BALF)by Enzyme-linked immunosorbent assay(ELISA),MUC5AC in lung tissue homogenate by ELISA,glutathione peroxidase(GSH-PX)in serum and BALF by spectrophotometry,and the expression of p-ERK1/2,p-JNK1/2 and p-p38 proteins by Western blot.All the measurements were analyzed and compared statistically.Results Lung tissue of rats exposed to PM2.5 showed histological destruction and increased mucus secretion of bronchial epithelial cells.Rats receiving NAC treatment showed less histological destruction and mucus secretion.Of P,L,M and H group,MUC5AC in lung tissue,IL-6 in serum and BALF were higher than controls(C1 and C2)(all P<0.05),with the highest levels found in the P group and a decreasing trend with increase of NAC dose.The activity of GSH-PX in serum and BALF of PM2.5 exposed rats(P,L,M and H)was lower than that of controls(all P<0.05),with higher activities found in NAC treated rats(L,M,and H),and an increasing trend with increase of NAC dose.The expressions of p-ERK1/2,p-JNK1/2 and p-p38 proteins in PM2.5 exposed lung tissue(P,L,M and H)was higher than controls(all P<0.05),with decreased levels and dose dependent downregulation found in NAC treated rats.Conclusion NAC can antagonize major MAPK pathway activation,lung oxidative stress and inflammatory injury induced by PM2.5 in rats.

Oxidative stress related enzymes in response to chromium(VI) toxicity in Oxya chinensis (Orthoptera: Acridoidae)

The toxic effects of Cr（Vl） on antioxidant enzymes of Oxya chinensis（Orthoptera： Acridoidae） were determined. Changes in the activities of the antioxidant enzymes superoxide dismutase（SOD）, catalase（CAT）, and guaiacol peroxidase（GPx） were measured in O. chinensis insects injected with Cr（VI）. Fifth-nymphs of O. chinensis insects were injected with Cr（VI） with different concentrations （0, 75, 150, 225, 300, 375, 450 mg/kg of body weight）. The results showed that Cr（VI） led to the change of SOD, CAT, and GPx activities at different concentrations, which revealed that： （1） The oxidative stress of SOD increased with the increase of Cr （VI） concentration. （2） With the increase of Cr （VI） concentrations, CAT activities for females increased at lower concentrations, but decreased at higher concentration range, which indicated that antioxidant system of O. chinensis was not influenced by the presence of Cr （VI）. A very similar response to Cr（VI） effect for males indicated that Cr（VI） concentrations were not high enough to damage O. chinensis in terms of CAT. （3） The GPx activity for females increased in all treatments, which revealed that the damage power of Cr（VI） was increased with the increase of Cr（Vi） concentrations in terms of GPx, but the effect was not so remarkable. There was not a consistent trend of GPx activities for males in all treatments of Cr（VI）. Cr（VI）-induced changes in antioxidant enzymes were different for SOD, CAT and GPx, of which the tendency was that activities generally changed with increase of concentrations of Cr（VI） suggesting SOD, CAT, and GPx could serve as indices of oxidative stress to some extent.

Comparison of physiological responses to oxidative and heavy metal stress in seedlings of rice paddy, Oryza sativa L.

Physiological responses on the bases of activities of antioxidant enzymes: peroxidase, catalase, superoxide dismutase and glutathione reductase as well as estimation of total protein, lipid peroxidation and thiols in the form of protein, non\|protein, glutathione and phytochelatin measured in growing seedlings of paddy, Oryza sativa L., from day 2 to 8 were compared following treatment of seeds for 5h with oxidative agents, paraquat 5 × 10 -5 , 10 -4 , 10 -3 mol/L, H 2O 2 10 -3 , 5×10 -3 , 10 -2 mol/L, and CdCl 2 10 -5 , 10 -4 , 5×10 -3 mol/L. A significant induction of all antioxidant enzymes along with an increase in the levels of protein, lipid peroxidation and glutathione was noted in response to oxidative stress, CdCl 2 induced significant peroxidase and catalase activities but not superoxide dismutase. In a marked contrast from oxidative stress, CdCl 2 decreased glutathione reductase activity as well as glutathione levels but increased phytochelatin level. The different physiological responses thus underlined the crucial involvement of glutathione and phytochelatin in the oxidative and heavy metal\|linduced adaptive responses respectively.

Programmed cell death, antioxidant response and oxidative stress in wheat f lag leaves induced by chemical hybridization agent SQ-1

Male sterility induced by a chemical hybridization agent （CHA） is an important tool for utilizing crop heterosis. Leaves, especially the flag leaves, as CHA initial recipients play a decisive role in inducing male sterility. To investigate effects of different treatment times of CHA-SQ-1 used, morphological, biochemical and physiological responses of wheat flag leaves were detected in thistudy. CHA induced programmed cell death （PCD） as shown in terminal deoxynucleotidyl transferase-mediated dUTP nick end-labelling （TUNEL） and DNA laddering analysis. In the early phase, CHA-SQ-1 trig- gered organelle changes arid PCD in wheat leaves accompanied by excess production of reactive oxygen species （O2- and H202） and down-regulation of the activities of superoxide dismutase （SOD）, catalase （CAT） and guaiacol peroxidase （POD）. Meanwhile, leaf cell DNAs showed ladder-like patterns on agarose gel, indicating that CHA-SQ-1 led to the activation of the responsible endonuclease. The oxidative stress assays showed that lipid peroxidation was strongly activated and photosynthesis was obviously inhibited in SQ-l-induced leaves. However, CHA contents in wheat leaves gradually reduced along with the time CHA-SQ-1 applied. Young flags returned to an oxidative/antioxidative balance and ultimately developed into mature green leaves. These results provide explanation of the relations between PCD and anther abortion and practical application of CHA for hybrid breeding.

Review of oxidative stress and antioxidative defense mechanisms in Gossypium hirsutum L.in response to extreme abiotic conditions

Oxidative stress occurs when crop plants are exposed to extreme abiotic conditions that lead to the excessive production and accumulation of reactive oxygen species(ROS).Those extreme abiotic conditions or stresses include drought,high temperature,heavy metals,salinity,and ultraviolet radiation,and they cause yield and quality losses in crops.ROS are highly reactive species found in nature that can attack plant organelles,metabolites,and molecules by interrupting various metabolic pathways until cell death occurs.Plants have evolved defense mechanisms for the production of antioxidants to detoxify the ROS and to protect the plant against oxidative damage.Modern researches in crop plants revealed that low levels of ROS act as a signal which induces tolerance to environmental extremes by altering the expression of defensive genes.In this review,we summarized the processes involved in ROS production in response to several types of abiotic stress in cotton plants.Furthermore,we discussed the achievements in the understanding and improving oxidative stress tolerance in cotton in recent years.Researches related to plant oxidative stresses have shown excellent potential for the development of stress-tolerant crops.

Thioredoxin interacting protein,a key molecular switch between oxidative stress and sterile inflammation in cellular response

Tissue and systemic inflammation have been the main culprit behind the cellular response to multiple insults and maintaining homeostasis.Obesity is an independent disease state that has been reported as a common risk factor for multiple metabolic and microvascular diseases including nonalcoholic fatty liver disease(NAFLD),retinopathy,critical limb ischemia,and impaired angiogenesis.Sterile inflammation driven by high-fat diet,increased formation of reactive oxygen species,alteration of intracellular calcium level and associated release of inflammatory mediators,are the main common underlying forces in the pathophysiology of NAFLD,ischemic retinopathy,stroke,and aging brain.This work aims to examine the contribution of the pro-oxidative and pro-inflammatory thioredoxin interacting protein(TXNIP)to the expression and activation of NLRP3-inflammasome resulting in initiation or exacerbation of sterile inflammation in these disease states.Finally,the potential for TXNIP as a therapeutic target and whether TXNIP expression can be modulated using natural antioxidants or repurposing other drugs will be discussed.

Ki20227 aggravates apoptosis,inflammatory response,and oxidative stress after focal cerebral ischemia injury

The survival of microglia depends on the colony-stimulating factor-1 receptor(CSF1R)signaling pathway under physiological conditions.Ki20227 is a highly selective CSF1R inhibitor that has been shown to change the morphology of microglia.However,the effects of Ki20227 on the progression of ischemic stroke are unclear.In this study,male C57 BL/6 mouse models of focal cerebral ischemic injury were established through the occlusion of the middle cerebral artery and then administered 3 mg/g Ki20227 for 3 successive days.The results revealed that the number of ionized calcium-binding adaptor molecule 1/bromodeoxyuridine double positive cells in the infarct tissue was reduced,the degree of edema was increased,neurological deficits were aggravated,infarct volume was increased,and the number of peri-infarct Nissl bodies was reduced.The number of terminal deoxynucleotidyl transferase dUTP nick-end labeling-positive cells in the peri-infarct tissue was increased.The expression levels of Bax and Cleaved caspase-3 were up-regulated.Bcl-2 expression was downregulated.The expression levels of inflammatory factors and oxidative stress-associated factors were increased.These findings suggested that Ki20227 blocked microglial proliferation and aggravated the pathological progression of ischemia/reperfusion injury in a transient middle cerebral artery occlusion model.This study was approved by the Animal Ethics Committee of Lanzhou University Second Hospital(approval No.D2020-68)on March 6,2020.

Oxidative Stress and Post-Ischemic Inflammatory Response in Ischemic Stroke Complicated with Diabetes Mellitus Type 2

Oxidative stress and post-ischemic inflammatory response are the key pathogenic mechanisms of the neuronal injury caused by ischemic stroke (IS). On the other hand, Diabetes is a major risk factor for the development of stroke, increasing the susceptibility to atherosclerosis and the prevalence of atherogenic risk factors, including hypertension, obesity, and abnormal blood lipids. The aim of current study was to analyze the functional activity of oxidant-antioxidant system and post-ischemic inflammatory response in IS patients complicated and noncomplicated with diabetes mellitus type 2 (DM2). ELISA, photochemiluminescent and spectrophotometric methods were used to analyze the serum samples of IS patients complicated and noncomplicated with DM2, DM2 patients, as well as healthy subjects. The results obtained suggest that IS complicated with diabetes is characterized by higher intensity of the lipid peroxidation process as compared to IS noncomplicated with diabetes that, probably, is one of the determining factors responsible for more severe clinical course of IS patients complicated with DM2 compared to those noncomplicated with DM2. It is also shown that mechanisms of the compensatory response to oxidative stress on the level of antioxidants in IS patients complicated with diabetes differ from those detected in IS noncomplicated with diabetes. A significant increase of the levels of the five analyzed cytokines in both groups of IS patients were detected. Based on the results obtained we suggest that metabolic, molecular, and cellular level alterations are typical for long-term DM2 impair compensatory mechanisms protecting the body from oxidative stress, and that in IS complicated with DM2 the systemic inflammatory reactions and oxidative stress are more intense than in case of IS noncomplicated with DM2.

Effects of DPP-4 inhibitor combined with metformin on blood glucose control, oxidative stress and inflammatory response in patients with type 2 diabetes mellitus

Objective: To investigate the effects of DPP-4 inhibitor combined with metformin on blood glucose control, oxidative stress and inflammatory response in patients with type 2 diabetes mellitus (T2DM). Methods: A total of 138 patients with newly diagnosed T2DM who were treated in the hospital between March 2016 and April 2017 were divided into routine group (n=69) and combined treatment group (n=69) by random number table method. Routine group were treated with metformin alone and combined treatment group received DPP-4 inhibitor combined with metformin therapy. The differences in blood glucose control as well as oxidative stress-related indicator and inflammatory factor contents were compared between the two groups before and after treatment. Results: Before treatment, the differences in blood glucose index levels in peripheral blood as well as the oxidative stress index and inflammatory mediator contents in serum were not statistically significant between the two groups. After 4 weeks of treatment, blood glucose indexes FBG and HOMA-IR levels in peripheral blood of combined treatment group were lower than those of routine group;oxidative stress indexes MDA and LHP contents in serum were lower than those of routine group whereas GSH-Px and T-AOC contents were higher than those of routine group;inflammatory mediators hs-CRP, IL-1 and IL-6 contents in serum were lower than those of routine group. Conclusion: DPP-4 inhibitor combined with metformin therapy can effectively control the blood glucose and suppress the systemic oxidative stress and inflammatory response in T2DM paients.

Effect of laparoscopic surgery and laparotomy on oxidative stressresponse and cell invasion in lesions after hysteromyomectomy

Objective: To study the effect of laparoscopic surgery and laparotomy on oxidative stress response and cell invasion in lesions after hysteromyomectomy. Methods: Patients with uterine fibroids who received surgical resection in our hospital between August 2014 and March 2017 were retrospectively analyzed and divided into laparoscopy group and laparotomy group according to different surgical procedures. Immediately after surgery and 24 h after surgery, the contents of oxidative stress response indexes in serum were measured;after surgical resection, the uterine fibroid lesion was collected to determine the expression of cell invasion indexes. Results: Serum MDA, NE, E, Cor and ACTH levels of laparoscopy group immediately after surgery and 24 h after surgery were significantly lower than those of laparotomy group while GSH-Px and T-SOD levels were significantly higher than those of laparotomy group;after surgical resection, CXCL12, CXCR4, MMP2, MMP7 and MMP9 mRNA expression in uterine fibroid lesions of laparoscopy group were significantly lower than those of laparotomy group while TIMP1, TIMP2, RECK and E-cadherin mRNA expression were significantly higher than those of laparotomy group. Conclusion: Laparoscopic surgery can reduce the oxidative stress response after hysteromyoma and inhibit the invasive growth of cells in the lesion.

Correlation of serum vitamin E content with insulin resistance and oxidative stress response in patients with type 2 diabetes mellitus

Objective: To study the correlation of serum vitamin E content with insulin resistance and oxidative stress response in patients with type 2 diabetes mellitus. Methods: Patients who were diagnosed with type 2 diabetes mellitus in Xining Second People's Hospital between February 2016 and February 2017 were selected as T2DM group, healthy volunteers who received physical examination during the same period were selected as control group, oral glucose tolerance test was conducted to detect insulin resistance indexes, and fasting venous blood was collected to detect oxidative stress indicators. Results: Serum VitE, 2 h-Ins, 2 h-CP, Trx, Txnip, SOD and GSH-Px levels of T2DM group were significantly lower than those of control group while F-Ins, F-CP, MDA, AOPP, 8-OHdG, AGEs and LOX-1 levels were significantly higher than those of control group;serum VitE level in T2DM patients was positively correlated with serum 2 h-Ins, 2 h-CP, Trx, Txnip, SOD and GSH-Px levels, and negatively correlated with serum F-Ins, F-CP, MDA, AOPP, 8-OHdG, AGEs and LOX-1 levels. Conclusion: The decrease of serum vitamin E in patients with type 2 diabetes mellitus can lead to the aggravation of insulin resistance and the activation of oxidative stress response.

Genome-wide transcriptional response of the Arctic bacteriumPseudoalteromonas sp. A2 to oxidative stress induced byhydrogen peroxide

Oxidative stress is one of the major challenges faced by Arctic marine bacteria due to the high oxygen concentration of seawater, low temperatures and UV radiations. Transcriptome sequencing was performed to obtain the key functional genes involved in the adaptation to oxidative stress induced by hydrogen peroxide in the Arctic bacterium Pseudoalteromonas sp. A2. Exposure to 1 mmol/L H2O2 resulted in large alterations of the transcriptome profile, including significant up-regulation of 109 genes and significant down-regulation of 174 genes. COG functional classification revealed that among the significantly regulated genes with known function categories, more genes belonging to posttranslational modification, protein turnover and chaperones were significantly up-regulated, and more genes affiliated with chaperones and amino acid transport and metabolism were significantly down-regulated. It was notable that the expressions of eighteen genes affiliated with flagella and four genes affiliated with heat shock proteins were significantly up-regulated. Meanwhile, the expression of nine genes belonging to cytochrome and cytochrome oxidase, and five genes belonging to Ton B-dependent receptor,were significantly down-regulated. Among the eighteen genes with antioxidant activity categorized by GO analysis, the expression of one gene was significantly up-regulated; however, the expressions of two genes were significantly down-regulated. Briefly, RNA-Seq indicated that, except for the classical anti-oxidative genes and stress proteins, genes affiliated with flagella and function unknown played important roles in coping with oxidative stress in Pseudoalteromonas sp. A2. This overall survey of transcriptome and oxidative stress-relevant genes can contribute to understand the adaptive mechanism of Arctic bacteria.

Effect of juglone on immunity response and oxidative stress in mice

To research juglone＇s immunology regulation, several perspectives including immunology regulation, lymphocyte proliferation, and cytokines were presented. The index of thymus and spleen, total supperoxide dismutase activity （T-SOD）, serum malondialdehyde （MDA）, content of nitrogen oxide （NO）, the anti-superoxide anion ability, the suppressing hydroxy radical ability, contents of reduced glutathione （GSH） in thymus, total antioxidationabiUty （T-AOC） and the level of mouse ly- sozyme （LZM） in plasma were measured. LPS-induced B thymocytes proliferation was measured by MTT assay. In the low-immunity model group, MDA and NO levels were decreased （p 〈0. 001）. Ju- glone improved lysozyme （LZM）, GSH contents in thymus, T-AOC, T-SOD activity, the anti-super- oxide anion ability （anti- O2-） （p 〈0. 001）. In the stimulation immunity model group, MDA and NO levels （p 〈0. 05）, anti- 02- and T-SOD activity （p 〈0. 05） were up-regulated, whereas LZM, T-AOC contents were down-regulated, juglone has a significant effect, which promotes cell regeneration and function recovery, also may alleviate oxidative damage; juglone possesses a dual regulating effect on humoral immunity in mice.

Effect of group psychological intervention on oxidative stress,apoptosis and inflammatory response in patients with schizophrenia

Objective: To investigate the effect of group psychological intervention on oxidative stress, apoptosis and inflammatory response in patients with schizophrenia. Methods: A total of 80 patients with schizophrenia who received hospitalization in the hospital between September 2014 and October 2016 were collected and divided into control group (n=40) and observation group (n=40) according to the random number table method. Control group received routine clinical intervention, the observation group received group psychological intervention on the basis of conventional intervention, and the differences in serum contents of oxidative stress indicators, apoptosis molecules and inflammatory factors were compared between the two groups of patients before and after intervention. Results: Before intervention, the differences in serum levels of oxidative stress indexes, apoptosis molecules and inflammatory factors were not statistically significant between the two groups of patients. After intervention, serum SOD and bcl-2 levels of both groups of patients were higher than those before intervention while MDA, bax, Caspace-3, Fas, IL-1β, IL-6 and TNF-α levels were lower than those before intervention, and serum SOD and bcl-2 levels of observation group were higher than those of control group while MDA, bax, Caspace-3, Fas, IL-1β, IL-6 and TNF-α levels were lower than those of control group. Conclusion: Group psychological intervention can effectively inhibit the systemic oxidative stress and inflammatory response, and reduce the process of apoptosis in patients with schizophrenia.

Effects of Guizhi Fuling Pill combined with metformin on insulin resistance-related inflammatory response and oxidative stress response in patients with PCOS

Objective: To study the effects of Guizhi Fuling Pill combined with metformin on insulin resistance-related inflammatory response and oxidative stress response in patients with polycystic ovary syndrome (PCOS). Methods: PCOS patients who received therapy in Panzhihua Maternal and Child Care Service Centre between June 2013 and February 2013 were selected and randomly divided into two groups, combined therapy group received Guizhi Fuling Pill combined with metformin therapy for two months, and metformin group received metformin therapy for continuous two months. After serum pickup, the follicular fluid was collected to determine the expression of insulin signaling pathway molecules as well as the protein levels of inflammatory response indexes and oxidative stress response indexes. Results:Serum IRS-1, IRS-2, PI3K, AKT and GLUT4 mRNA expression of combined therapy group were greatly higher than those of metformin group whereas GSK-3β mRNA expression was significantly lower than that of metformin group;serum NF-kB, TNF-α, IL-6, IL-18, MCP-1, ROS, MDA and 8-OHdG protein levels of combined therapy group were greatly below those of metformin group and negatively correlated with IRS-1 and IRS-2 mRNA expression whereas TAC and SOD levels were higher than those of metformin group and positively correlated with IRS-1 and IRS-2 mRNA expression. Conclusion: Guizhi Fuling Pill combined with metformin can reduce the inflammatory response and oxidative stress response to improve the insulin resistance and increase the insulin sensitivity in patients with PCOS.

Effect of sequential mechanical ventilation on cardiac function, endothelial injury and oxidative stress response in patients with cor pulmonale

Objective: To study the effect of sequential mechanical ventilation on cardiac function, endothelial injury and oxidative stress response in patients with cor pulmonale (CCP). Methods: Patients with cor pulmonale complicated by respiratory failure who were treated in Dongfeng People's Hospital between May 2014 and February 2017 were selected and randomly divided into the sequential group who received sequential mechanical ventilation combined with conventional therapy and the control group who received invasive positive pressure ventilation combined with conventional therapy. The serum levels of cardiac function-related neurohumoral indicators, endothelial injury indicators and oxidative stress response indicators were detected before treatment as well as 3 d and 7 d after treatment. Results: 3 d and 7 d after treatment, serum NT-proBNP, Copeptin, Ang-II, ALD, ET-1, vWF, sST2 levels of both groups of patients were significantly lower than those before treatment while NO, SOD, GSH-Px and T-AOC levels were significantly higher than those before treatment;serum NT-proBNP, Copeptin, Ang-II, ALD, ET-1, vWF, sST2, NO, 8-iso-PGF2a, MDA, SOD, GSH-Px and T-AOC levels of sequential group 3 d after treatment were not significantly different from those of control group;serum NT-proBNP, Copeptin, Ang-II, ALDET-1, vWF, sST2, 8-iso-PGF2a and MDA levels of sequential group 7 d after treatment were significantly lower than those of control group while NO, SOD, GSH-Px and T-AOC levels were significantly higher than those of control group. Conclusion: Sequential mechanical ventilation for cor pulmonale can improve the cardiac function and reduce the degree of endothelial injury and oxidative stress response.

Oxidative Stress and Inflammatory Response in Early Stage of Diffuse Axonal Injury in Rats

Objective: To investigate the role of oxidative stress and immunoinflammatory reaction in early stage of diffuse axonal injury (DAI). Methods: 96 adult male SD rats were divided into 2 groups (n = 48 in each): sham group and DAI group. Rat diffuse axonal injury was induced by a rat instant lateral head rotation device, which was developed to let the rat head spin 90 degree at the moment to cause shearing injury. The modified neurological severity score (mNSS), histomorphology, PI staining, GFAP immunofluorescent staining, SOD activity, CAT activity, MDA content and western blotting (IL-6,IL-1, JNK and p-JNK) in parietal cortex were investigated at 6 h, 1 d and 3 d after DAI. Results: The neurological severity scores, GFAP positive cell, PI positive cells, MDA, IL-6, IL-1, JNK and p-JNK were significantly increased and the SOD and CAT activities were decreased after DAI. Conclusion: Oxidative stress and immunoinflammatory reaction played important roles in DAI pathophysiological process in acute phase.