Minocycline in the eradication of Helicobacter pylori infection: A systematic review and meta-analysis

BACKGROUND Difficulty in obtaining tetracycline,increased adverse reactions,and relatively complicated medication methods have limited the clinical application of the classic bismuth quadruple therapy.Therefore,the search for new alternative drugs has become one of the research hotspots.In recent years,minocycline,as a semisynthetic tetracycline,has demonstrated good potential for eradicating Helicobacter pylori(H.pylori)infection,but the systematic evaluation of its role remains lacking.AIM To explore the efficacy,safety,and compliance of minocycline in eradicating H.pylori infection.METHODS We comprehensively retrieved the electronic databases of PubMed,Embase,Web of Science,China National Knowledge Infrastructure,SinoMed,and Wanfang database as of October 30,2023,and finally included 22 research reports on H.pylori eradication with minocycline-containing regimens as per the inclusion and exclusion criteria.The eradication rates of H.pylori were calculated using a fixed or a random effect model,and the heterogeneity and publication bias of the studies were measured.RESULTS The single-arm meta-analysis revealed that the minocycline-containing regimens achieved good overall H.pylori eradication rates,reaching 82.3%[95%confidence interval(CI):79.7%-85.1%]in the intention-to-treat analysis and 90.0%(95%CI:87.7%-92.4%)in the per-protocol analysis.The overall safety and compliance of the minocycline-containing regimens were good,demonstrating an overall incidence of adverse reactions of 36.5%(95%CI:31.5%-42.2%).Further by traditional meta-analysis,the results showed that the minocycline-containing regimens were not statistically different from other commonly used eradication regimens in eradication rate and incidence of adverse effects.Most of the adverse reactions were mild to moderate and well-tolerated,and dizziness was relatively prominent in the minocycline-containing regimens(16%).CONCLUSION The minocycline-containing regimens demonstrated good efficacy,safety,and compliance in H.pylori eradication.Minocycline has good potential to replace tetracycline for eradicating H.pylori infection.

Effect of minocycline and its nano-formulation on central auditory system in blast-induced hearing loss rat model

Blast injuries are common among the military service members and veterans.One of the devastating effects of blast wave induced TBI is either temporary or permanent hearing loss.Treating hearing loss using minocycline is restricted by optimal drug concentration,route of administration,and its half-life.Therefore,therapeutic approach using novel therapeutic delivery method is in great need.Among the different delivery methods,nanotechnology-based drug delivery is desirable,which can achieve longer systemic circulation,pass through some biological barriers and specifically targets desired sites.The current study aimed to examine therapeutic effect of minocycline and its nanoparticle formulation in moderate blast induced hearing loss rat model through central auditory system.The I.v.administered nanoparticle at reduced dose and frequency than regularly administered toxic dose.After moderate blast exposure,rats had hearing impairment as determined by ABR at 7-and 30-days post exposure.In chronic condition,free minocycline also showed the significant reduction in ABR threshold.In central auditory system,it is found in this study that minocycline nanoparticles ameliorate excitation in inferior colliculus;and astrocytes and microglia activation after the blast exposure is reduced by minocycline nanoparticles administration.The study demonstrated that in moderate blast induced hearing loss,minocycline and its nanoparticle formulation exhibited the optimal therapeutic effect on the recovery of the ABR impairment and a protective effect through central auditory system.In conclusion,targeted and non-targeted nanoparticle formulation have therapeutic effect on blast induced hearing loss.

Morbihan disease misdiagnosed as senile blepharoptosis and successfully treated with short-term minocycline and ketotifen: A case report

BACKGROUND Morbihan disease is a rare skin condition with diagnostic and therapeutic challenges.Facial nonpitting erythematous edema is usually considered to be a characteristic manifestation and diagnostic clue for the Morbihan disease.Treatment of Morbihan disease remains a dilemma due to its long course,poor response,and high recurrence rate.CASE SUMMARY We report the case of a 69-year-old man with Morbihan disease.The patient presented ptosis as the first and main symptom.There was no obvious edema or other skin lesions.The patient was misdiagnosed with senile blepharoptosis based on eyelid performance and no treatment was administered to him.After continuous progressive asthenia of eye-opening and ptosis for more than one year,a skin biopsy was recommended.Histopathological analysis showed edema in the dermis,lymphatic hyperplasia and dilatation,and perivascular lymphocytic infiltration.An obvious increase in toluidine blue-stained mast cells was observed.The patient was finally diagnosed with Morbihan disease.Minocycline and ketotifen were prescribed based on the increase of mast cells in skin tissue slices.The patient experienced rapid relief seven days later and complete remission after 40 d from the commencement of the treatment.CONCLUSION Ptosis without obvious swelling could be the only or main clinical manifestation of Morbihan disease in rare conditions.An increase of mast cells was an important therapeutic clue to the rapid and remarkable efficiency of the combination therapy of minocycline and antihistamine.

Minocycline attenuates cognitive impairment and restrains oxidative stress in the hippocampus of rats with chronic cerebral hypoperfusion

Objective Nitric oxide （NO） was speculated to play an Minocycline, a tetracycline derivative, reduced inflammation important role in the pathophysiology of cerebral ischemia. and protected against cerebral ischemia. To study the neuroprotection mechanism of minocycline for vascular dementia, the influences of minocycline on expressions of inducible nitric oxide synthase （iNOS） and endothelial nitric oxide synthase （eNOS） were observed in the brains of Wistar rats. Methods The vascular dementia rat model was established by permanent bilateral common carotid arteries occlusion （BCCAO）. Wistar rats were divideded into 3 groups randomly： sham-operation group （S group）, vascular dementia model group （M group）, and minocycline treatment group （MT group）. The behaviour was tested with Morris water maze and open-field task. Expressions of iNOS and eNOS were measured by immunohistochemistry and reverse transcriptase-polymerase chain reaction （RT-PCR）. The optical density value was measured by imaging analysis. Percentage of positive ceils with iNOS and eNOS expression was analyzed with optical microscope. Results Minocycline attenuated cognitive impairment. Inducible NOS was significantly down-regulated in MT group, compared with that in M group （P 〈 0.01）, while eNOS was significantly up-regulated, compared with that in M group （P 〈 0.01）. The expressions of iNOS and eNOS in M and MT groups were higher than those in S group （P 〈 0.01）. Conclusion Minocycline can down-regulate the expression of iNOS and up-regulate the expression of eNOS in vascular dementia, which restrains apoptosis and oxidative stress to protect neural function.

Minocycline对Lactacystin大鼠模型黑质胶质活化和多巴胺神经元生存的干预作用

目的:观察米诺环素(Minocycline,Mino)对Lactacystin(Lac)模型黑质内胶质细胞反应和多巴胺神经元的干预作用。方法:成年SD大鼠30只随机分为对照、Lac1 W、Lac3 W、Lac5 W、Lac+Mino5 W组,进行Lac动物模型制备和Mino给药处理,通过免疫组织化学和Western blot方法,观察iba1(小胶质细胞标志物)、GFAP(星形胶质细胞标志物)、TH(多巴胺能神经元标志物)的表达水平或阳性细胞数量变化,分析评价黑质内胶质细胞反应和多巴胺神经元生存状态。结果:Lac处理模型黑质内胶质细胞呈现动态活化反应。与生理盐水对照组相比,Lac处理均诱导iba1和GFAP表达水平升高,iba1在Lac3 W组显著升高、并持续高水平至Lac5 W(P<0.05)。GFAP表达在Lac1 W已显著升高、维持至Lac3 W和Lac5 W(P<0.05)。伴随胶质细胞的显著活化反应,黑质内TH阳性神经元数量急剧减少(P<0.01)。与Lac5 W组相比,Lac+Mino5 W组呈现对iba1和GFAP阳性胶质细胞的抑制效应、并提高黑质内TH阳性细胞数量,具有统计学意义(P<0.05)。结论:小胶质细胞抑制剂米诺环素给药处理可能通过干扰胶质细胞的异常活化反应、发挥对Lac损伤模型黒质多巴胺能神经元的一定保护作用。

Minocycline降低耳蜗毛细胞内蛋白质硝基反应拮抗链霉素耳毒性的研究

目的观察minocycline对链霉素诱导的耳毒性的拮抗作用。方法选用新生4天的Wistar大鼠60只，分离耳蜗进行离体培养。随机分为4组，包括正常培养的对照组，100μmol／L的minocycline作用组，500umol／L的硫酸链霉素作用组，100μmol／L的minocycline预处理6h然后500μmol／L的硫酸链霉素作用组。采用F-actin标记毛细胞纤毛观察毛细胞存活情况。免疫组织化学染色法检测耳蜗基底膜3一硝基酪氨酸的表达。Western Bloting检测耳蜗组织中iNos、3-硝基酪氨酸（3-nitrotyrosine，3-NT）的表达。结果500umol／L的链霉素作用24h后毛细胞出现缺失，从顶回至底回逐渐严重。支持细胞未见异常。免疫组化结果显示3-NT在毛细胞区域呈阳性表达。Minocycline预处理组能够提高链霉素作用后的毛细胞存活率，并且minocycline显著降低耳蜗组织由链霉素引起的iNOSS和3-NT蛋白过表达。结论minocycline对链霉素所致的耳蜗毛细胞损伤有拮抗作用，其机制可能部分通过抑SrJNO的过度生成，以减少耳蜗细胞内过氧亚硝基阴离子（ONOO-）产生的蛋白质硝基化反应。

Minocycline对rhHGF刺激ECV304细胞株表达MMP9的抑制作用

目的探讨重组人类肝细胞增殖因子(recombinant human hepatocyte growth factor,rhHGF)刺激ECV304细胞株表达基质金属蛋白酶-9(matrjx metalloproteinase-9,MMP-9)的作用及米诺环素(minocycline)的影响作用.方法绘制正常ECV304细胞株生长曲线,明确最适生长浓度及对数生长期;明确rhHGF及minocycline的作用浓度;流式细胞仪(flow cytometer,FCM)检测ECV304细胞株的MMP-9水平.结果①ECV304细胞株的最适生长浓度为1.0E+4/mL,对数生长期为3～5d;rhHCF的作用浓度为8ng/mL,minocycline的作用浓度为1.0E-5mol/L.②对照组MMP-9的表达量为39.74%;培养基中加入rhHGF8ng/mL后,细胞存活率为1.388169±0.102033(P＜0.01),MMP-9的表达量为40.32%;培养基中加入minocycline1.0E5mol/L后,细胞存活率为0.294526±0.076829(P＜0.01),MMP-9的表达量为19.92%.③培养基中加入minocycline 1.0E5mol/L 15min后加入rhHGF 8ng/mL,细胞存活率为0.397291±0.099504(P＜0.01),MMP-9的表达量为22 28%.结论rhHGF可刺激ECV304细胞株增殖,使MMP-9的表达量增加;minocycline可抑制ECV304细胞株增殖,使MMP-9的表达量降低;minocycline可拮抗rhHGF所引起的ECV304细胞株增殖,从而使MMP-9的表达量降低.

Neuroprotective effects of minocycline on focal cerebral ischemia injury: a systematic review

To review the neuroprotective effects of minocycline in focal cerebral ischemia in animal models.By searching in the databases of PubMed,ScienceDirect,and Scopus,and considering the inclusion and exclusion criteria of the study.Studies were included if focal cerebral ischemia model was performed in mammals and including a control group that has been compared with a minocycline group.Written in languages other than English;duplicate data;in vitro studies and combination of minocycline with other neuroprotective agents were excluded.Neurological function of patients was assessed by National Institute of Health Stroke Scale,modified Rankin Scale,and modified Barthel Index.Neuroprotective effects were assessed by detecting the expression of inflammatory cytokines.We examined 35 papers concerning the protective effects of minocycline in focal cerebral ischemia in animal models and 6 clinical trials which had evaluated the neuroprotective effects of minocycline in ischemic stroke.These studies revealed that minocycline increases the viability of neurons and decreases the infarct volume following cerebral ischemia.The mechanisms that were reported in these studies included anti-inflammatory,antioxidant,as well as anti-apoptotic effects.Minocycline also increases the neuronal regeneration following cerebral ischemia.Minocycline has considerable neuroprotective effects against cerebral ischemia-induced neuronal damages.However,larger clinical trials may be required before using minocycline as a neuroprotective drug in ischemic stroke.

Minocycline targets multiple secondary injury mechanisms in traumatic spinal cord injury

Minocycline hydrochloride（MH）, a semi-synthetic tetracycline derivative, is a clinically available antibiotic and anti-inflammatory drug that also exhibits potent neuroprotective activities. It has been shown to target multiple secondary injury mechanisms in spinal cord injury, via its anti-inflammatory, anti-oxidant, and anti-apoptotic properties. The secondary injury mechanisms that MH can potentially target include inflammation, free radicals and oxidative stress, glutamate excitotoxicity, calcium influx, mitochondrial dysfunction, ischemia, hemorrhage, and edema. This review discusses the potential mechanisms of the multifaceted actions of MH. Its anti-inflammatory and neuroprotective effects are partially achieved through conserved mechanisms such as modulation of p38 mitogen-activated protein kinase（MAPK） and phosphoinositide 3-kinase（PI3K）/Akt signaling pathways as well as inhibition of matrix metalloproteinases（MMPs）. Additionally, MH can directly inhibit calcium influx through the N-methyl-D-aspartate（NMDA） receptors, mitochondrial calcium uptake, poly（ADP-ribose） polymerase-1（PARP-1） enzymatic activity, and iron toxicity. It can also directly scavenge free radicals. Because it can target many secondary injury mechanisms, MH treatment holds great promise for reducing tissue damage and promoting functional recovery following spinal cord injury.

Effect of minocycline on cerebral ischemia-reperfusion injury

Minocylcine, a tetracycline derivate, has been shown to cross the blood-brain barrier and enter the central nervous system. In this study, cerebral ischemia-reperfusion injury models were established using the suture method, and minocycline was immediately injected intraperitoneally after cerebral ischemia-repeffusion （22.5 mg/kg, initially 45 mg/kg） at a 12-hour interval. Results showed that after minocycline treatment, the volume of cerebral infarction was significantly reduced, the number of surviving cell in the hippocampal CA1 region increased, the number of apoptotic cells decreased, the expression of caspase-3 and poly（adenosine diphosphate-ribose） polymerase-1 protein was down-regulated, and the escape latency in the water maze test was significantly shortened compared with the ischemia-reperfusion group. Our experimental findings indicate that minocycline can protect against neuronal injury induced by focal ischemia-reperfusion, which may be mediated by the inhibition of caspase-3 and poly（adenosine diphosphate-ribose） polymerase-1 protein expression.

Effects of minocycline on learning and memory of mice following ischemic-hypoxic cerebral injuries

An ischemic-hypoxic animal model was established using right common carotid artery occlusions and inhalation of low concentrations of oxygen in mice. At 10 days after the ischemic-hypoxic injuries, saline-treated mice exhibited significantly prolonged escape latencies in water-maze tests and significantly shorter memory latencies and more mistakes in step-down tests. In contrast, mice treated with 5 mg/kg minocycline exhibited significant reversals of each of these effects compared with the saline-treated control mice. Moreover, we found that minocycline can relieve brain water content and morphological changes in mice following ischemic-hypoxic cerebral injuries. Accordingly, our findings indicate that minocycline provides some protections against the deleterious effects of these injuries in mice.

Effects of minocycline on apoptosis and angiogenesis-related protein expression in a rat model of intracerebral hemorrhage

In the present study, a rat model of non-traumatic intracerebral hemorrhage was established by type IV collagenase injection into the right globus pallidus. Bax and Bcl-2 expression in tissues surrounding hematomas was significantly increased within 14 days after injury, and it then gradually decreased. Vascular endothelial growth factor, Flk-1 and Flt-1 mRNA expression gradually increased over time. After intraperitoneal injection with minocycline, Bax expression was decreased 1 day after intracerebral hemorrhage. Flk-1 and Flt-1 mRNA expression was decreased after minocycline injection, but Bcl-2 expression was increased, and vascular endothelial growth factor mRNA expression was decreased between 4-14 days. These results indicated that protective effects of minocycline on nerve tissues were associated with increased Bcl-2 expression and decreased Bax expression in the early stage after intracerebral hemorrhage. In the late stage, minocycline downregulated vascular endothelial growth factor and its receptor expression to inhibit brain tissue self-repair.

Antimicrobial Activity of Minocycline-Loaded Genipin-Crosslinked Nano-Fibrous Chitosan Mats for Guided Tissue Regeneration

Antimicrobial delivery has been advocated for guided tissue regeneration (GTR) or guided bone regeneration (GBR) therapies involving patients with aggressive or unresolved periodontitis/peri-implantitis. Electrospun chitosan membranes demonstrate several advantages over traditional GTR barrier membranes because they stimulate healing, mimic the topology of the extracellular matrix, and allow for diffusion of nutrients and wastes into/out of the graft site, and were shown to stimulate bone formation in a rabbit calvarial criticalsize defect model. Previously, we have shown improvements in mechanical properties and degradation kinetics by crosslinking electrospun membranes with 5 mM or 10 mM genipin. We have also demonstrated the ability of elecrospun chitosan membranes to inhibit lippopolysaccharide (LPS)-induced monocyte activation. In this study, minocycline was incorporated into the chitosan membrane by passive absorption at 5 or 10 mg/mL. The minocycline-loaded membranes and control membranes (carrier only) were tested against Porphyromonas gingivalis (P. gingivalis) by repeated zone of inhibition (ZOI) measurements. Testing showed that uncrosslinked and genipin-crosslinked membranes have similar capacity to absorb aqueous solutions (swelling ratio 1.7 - 2.2). Minocycline loading resulted in bacterial inhibition for up to 8 days from crosslinked membranes (with 11 mm initial ZOI) whereas uncrosslinked membranes loaded with minocycline only inhibited bacteria for 4 days (with 8 mm initial ZOI). These in vitro results suggest that genipin-crosslinked electrospun chitosan membranes loaded with minocycline may be able to reduce early bacterial contamination of GTR graft sites.

Effects of minocycline on apoptosis and neuronal changes in retinal ganglion cells from experimental optic neuritis rats

BACKGROUND： Minocycline, a tetracycline derivative, is neuroprotective in models of various neurological diseases. OBJECTIVE： To investigate the effects of minocycline on retinal ganglion cells （RGCs） in rats with optic neuritis, and to compare with the effects of methylprednisolone. DESIGN, TIME AND SETTING： This neuropathology controlled study was performed at the First Affiliated Hospital, Chongqing Medical University, China in May 2007. MATERIALS： A total of 22 female Wistar rats were randomly assigned into a normal control group （n ： 5） and an experimental group （n = 17）. The experimental group was composed of a model subgroup （n = 7）, a minocycline subgroup （n = 5）, and a methylprednisolone subgroup （n = 5）. Minocycline was supplied by Sigma, USA. METHODS： Antigen homogenate made from guinea pig spinal cord and complete Freund adjuvant was used to induce autoimmune encephalomyelitis, which could induce demyelinated optic neuritis models. Rats in the minocycline subgroup were intraperitoneally injected with minocycline （45 mg/kg） daily from day 8 following autoimmunity. Rats in the methylprednisolone subgroup were intraperitoneally injected with methylprednisolone （20 mg/kg） daily from day 8 following autoimmunity. MAIN OUTCOME MEASURES： On day 18 after autoimmunily induction, pathological changes in the optic nerve were observed by hematoxylin-eosin staining. The percentage area of axons in the transverse section of the optic nerve was measured by Bielschowsky staining. Apoptosis of RGCs was detected by TUNEL. RESULTS： Under an optical microscope, the optic nerve in rats with demyelinated optic neuritis showed a vacuole-like structure of fibers, irregular swelling of the axons, and infiltration of a large quantity of inflammatory cells. With an electron microscope, the optic nerve presented with vacuole-like structures in the axons, a small percentage area of axons in the transverse section, loose myelin sheaths, and microtubules and microfilaments disappeared. The pathological changes in the optic nerve met the changes in demyelinated optic neuritis. Moreover, there was significant apoptosis of RGCs. The percentage area of optic nerve axons in the transverse section was significantly increased and the number of apoptotic RGCs was increased after treatment with methylprednisolone and minocycline. Compared with methylprednisolone, minocycline had better effects on reducing RGC apoptosis （P 〈 0.05）. CONCLUSION： Minocycline has better inhibitory effects on RGC apoptosis than methylprednisolone. Minocycline can decrease the damage to axons of demyelinated optic neuritis rats, and has similar protective effects on neurons from demyelinated optic neuritis rats as methylprednisolone.

Effect of Minocycline Postconditioning and Ischemic Postconditioning on Myocardial Ischemia-reperfusion Injury in Atherosclerosis Rabbits

This study examined the protective effect of ischemic postconditioning(IPoC) and minocycline postconditioning(MT) on myocardial ischemia-reperfusion(I/R) injury in atherosclerosis(AS) animals and the possible mechanism.Forty male healthy rabbits were injected with bovine serum albumin following feeding on a high fat diet for 6 weeks to establish AS model.AS rabbits were randomly divided into 3 groups:(1) I/R group,the rabbits were subjected to myocardial ischemia for 35 min and then reperfusion for 12 h;(2) IPoC group,the myocardial ischemia lasted for 35 min,and then reperfusion for 20 s and ischemia for 20 s [a total of 3 cycles(R20s/I20s×3)],and then reperfusion was sustained for 12 h;(3) MT group,minocycline was intravenously injected 10 min before reperfusion.The blood lipids,malondialdehyde(MDA),superoxide dismutase(SOD),soluble cell adhesion molecule(sICAM),myeloperoxidase(MPO),and cardiac troponin T(cTnT) were biochemically determined.The myocardial infarction size(IS) and apoptosis index(AI) were measured by pathological examination.The expression of bcl-2 and caspase-3 was detected in the myocardial tissue by using reverse transcription-polymerase chain reaction(RT-PCR).The results showed that the AS models were successfully established.The myocardial IS,the plasma levels of MDA,sICAM,MPO and cTnT,and the enzymatic activity of MPO were significantly decreased,and the plasma SOD activity was significantly increased in IPoC group and MT group as compared with I/R group(P<0.05 for all).The myocardial AI and the caspase-3 mRNA expression were lower and the bcl-2 mRNA expression was higher in IPoC and MT groups than those in I/R group(all P<0.05).It is concluded that the IPoC and MT can effectively reduce the I/R injury in the AS rabbits,and the mechanisms involved anti-oxidation,anti-inflammation,up-regulation of bcl-2 expression and down-regulation of caspase-3 expression.Minocycline can be used as an effective pharmacologic postconditioning drug to protect myocardia from I/R injury.

Minocycline inhibits neuroinflammation and enhances vascular endothelial growth factor expression in a cerebral ischemia/reperfusion rat model

BACKGROUND： Brain ischemia involves secondary inflammation, which significantly contributes to the outcome of ischemic insults. Vascular endothelial growth factor （VEGF） may play an important role in the vascular response to cerebral ischemia, because ischemia stimulates VEGF expression in the brain, and VEGF promotes formation of new cerebral blood vessels. Minocycline, a tetracycline derivative, protects against cerebral ischemia and reduces inflammation, oxidative stress, and apoptosis. OBJECTIVE： To observe the influence of minocycline on VEGE interleukin-1 beta （IL-119 ）, and tumor necrosis factor alpha （TNF-α） expression in Wistar rats with focal cerebral ischemia/reperfusion injury, and to study the neuroprotection mechanism of minocycline against focal cerebral ischemia/reperfusion injury. DESIGN, TIME AND SETTING： Randomized, controlled experiment, which was performed in the Chongqing Key Laboratory of Neurology between March 2007 and March 2008. MATERIALS： A total of 36 female, Wistar rats underwent surgery to insert a thread into the left middle cerebral artery. Animals were randomly divided into sham-operation, minocycline treatment, and ischemia/reperfusion groups, with 12 rats in each group. Minocycline （Huishi Pharmaceutical Limited Company, China） was dissolved to 0.5 g/L in normal saline. METHODS： A 0.5-1.0 cm thread was inserted into rats from the sham-operation group. Rats in the ischemia/reperfusion group underwent ischemia and reperfusion. The minocycline group received minocycline （50 mg/kg） 12 and 24 hours following ischemia and reperfusion, whereas the other groups received saline at the corresponding time points. MAIN OUTCOME MEASURES： mRNA and protein expression of IL-1β and TNF-α was measured by reverse transcriptase-polymerase chain reaction （RT-PCR） and enzyme linked immnnosorbent assay （ELISA）, respectively. VEGF mRNA and protein expression was examined by RT-PCR, Western blot, and ELISA. RESULTS： Minocycline decreased the focal infarct volume. VEGF, IL-1β, and TNF-α expression was upregulated in the ischemia-perfusion group after injury. Following minocycline treatment, IL-1β and TNF- α expression was significantly downregulated, and VEGF was significantly upregulated, compared with the ischemia/reperfusion group （all P 〈 0.01）. Expression of VEGF, IL-1β, and TNF- α was greater in the ischemia-perfusion and minocycline treatment groups, compared with sham-operated animals （P 〈 0.01 ）. CONCLUSION： Minocycline can reduce expression of IL- 1β and TNF-α, and increase VEGF expression, in the rat brain following cerebral ischemia/reperfusion. From these findings, a hypothesis can be formed that minocycline attenuates neuroinflammation and enhances recovery of vascular integrity during the process of cerebral ischemia/reperfusion.

Minocycline for Schizophrenia: A critical review

Minocycline, an antibiotic of the tetracycline family, has been shown to display neurorestoractive or neuroprotective properties in various models of neurodegenerative diseases. In particular, it has been shown to delay motor alterations, inflammation and apoptosis in models of Huntington’s disease, amyotrophic lateral sclerosis and Parkinson’s disease. Despite controversies about its efficacy, the relative safety and tolerability of minocycline have led to the launching of various clinical trials. Previously, we reported the antipsychotic effects of minocycline in patients with schizophrenia. In a pilot investigation, we administered minocycline as an open-label adjunct to antipsychotic medication to patients with schizophrenia. The results of this trial suggested that minocycline might be a safe and effective adjunct to antipsychotic medications, and that augmentation with minocycline may prove to be a viable strategy for “boosting” antipsychotic efficacy and for treating schizophrenia. Recently, in randomized double-blind placebo-controlled clinical trials, the addition of minocycline to treatment as usual early in the course of schizophrenia predominantly improves negative symptoms. The present review summarizes the available data supporting the clinical testing of minocycline for patients with schizophrenia. In addition, we extend our discussion to the potential applications of minocycline for combining this treatment with cellular and molecular therapy.

Minocycline protects the apoptosis of PC12 cells induced by 1-methyl-4-phenylpyridinium

Objective： To explore the protective effect of minocycline on the apoptosis of cellular parkinsonism models induced by MPP^＋ . Methods： Using PC12 cells as the apoptotic model of dopaminergic neurons, MC and MPP^＋ were added into the culture medium of PC12 cells, and using MTr to assay the cell viability and metabolic state; The cells apoptosis was assayed by electrophoresis method and using flow cytometry FACS to assay the apoptosis ratio. Results： Added the MPP^＋ to get the concentration of 10μmol/L, the cellular parkinsonism model of apoptosis had been prepared. The pre-treatment of MC （ 100/μmol/L） could significantly increase the PC12 cell viability. The apoptosis ratio of MC＋MPP^＋ group was significantly lower than that of MPP^＋ group, but was still significantly higher than that of control group. Conclusion： MC may protect the cell apoptosis induced by MPP^＋ to some extent.

Effects of minocycline combined with periocline on the levels of inflammatory factors, ALP and NO in gingival crevicular fluid of patients with periodontitis

Objective:To investigate the effect of minocycline combined with periocline on patients with periodontitis, and analyze the effect of inflammatory factors, ALP and NO levels in the gingival sulcus fluid.Methods:A total of 100 cases of patients with periodontitis admitted in our hospital from December 2016 to May 2017, with a total of 128 teeth. They were divided into control group and observation group by the random number method, 64 teeth in each group. Patients in both groups were given conventional supragingival scaling and subgingival curettage therapy. The control group patients were given minocycline ointment in periodontal pockets until overflow, once a week;the observation group was given periocline treatment on the basis of control group. Oral administration 2 capsules each time, 2 times each day. The two groups were both treated for 4 weeks. The general indicators of teeth in both groups were compared. The levels of inflammatory factors, ALP and NO in gingival crevicular fluid of the two groups were detected before and after the treatment.Results: Before treatment, there was no significant difference in the levels of PLI, PD, SBI, AL and TNF-α, CRP, ALP and NO in the gingival crevicular fluid of the both groups. After treatment, the levels of PLI, PD, SBI, AL and TNF-α, CRP, ALP and NO in the gingival crevicular fluid of the two groups were significantly decreased than those before the treatment, and the levels of PLI, PD, SBI, AL and TNF-α, CRP, ALP and NO in gingival crevicular fluid after treatment in the observation group were all significantly lower than that in the control group after treatment, the differences were statistically significant.Conclusion: Minocycline combined with periocline can improve the periodontal condition and gingival crevicular fluid inflammatory state in patients with periodontitis, reduce the activity of ALP and NO. It has the effect of antiseptic and induced osteogenesis and improving the clinical effect.

Effects of minocycline on the expression of NGF and HSP70 and its neuroprotection role following intracerebral hemorrhage in rats

The present study was aimed to investigate the effects of minocycline （MC） on the expression of nerve growth factor （NGF） and heat shock protein 70 （HSP70） following intracerebral hemorrhage （ICH） in rats, and explore the neuroprotective function of MC. Seventy-eight male SD rats were randomly assigned to three groups： the ICH control group （n = 36）, ICH intervention group （n = 36） and sham operation group （n = 6）. The ICH control group and ICH intervention group were subdivided into 6 subgroups at 1, 2, 4, 5, 7 and 14 d after ICH with 6 rats in each subgroup. Type IV collagenase was injected into the basal nuclei to establish the ICH model. All rats showed symptoms of the nervous system after the model was established, and the sympotsm in the ICH control group were more serious than the ICH intervention group. The number of NGF-positive cells and HSP70-positive cells in the ICH intervention group was higher than that of the ICH control group. MC administration by intraperitoneal injection can increase the expression of NGF and HSP70. MC may inhibit the activation of microglia, the inflammatory reaction and factors, matrix metalloproteinases and apoptosis, thus protecting neurons. The change of the expression of NGF and HSP70 may be involved in the pathway of neuroprotection by MC.