黄芪多糖对2型糖尿病合并脓毒症大鼠胰腺线粒体氧化应激损伤的保护作用

目的探讨黄芪多糖(APS)对2型糖尿病(T2DM)合并脓毒症大鼠胰腺线粒体的氧化应激损伤的保护作用。方法 45只大鼠随机分为正常对照(C)组、假手术(S)组、生理盐水(N)组、小剂量APS(A1)组和大剂量APS(A2)组。高脂饲料喂养4周后,采用链脲佐菌素(STZ,30 mg/kg)制备T2DM大鼠模型,用盲肠结扎穿孔法复制脓毒症模型。观测胰腺线粒体中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活力,丙二醛(MDA)、一氧化氮(NO)含量。结果与N组比较,A1和A2组大鼠胰腺线粒体SOD、GSH-Px活力明显升高(P<0.05),而NO、MDA含量明显降低(P<0.05)。与C组相比,N组胰腺线粒体NO、MDA含量升高(P<0.05),SOD、GSH-Px活力水平降低(P<0.05)。结论 T2DM合并脓毒症大鼠胰腺线粒体氧化应激损伤严重,黄芪多糖能有效减轻其氧化应激损伤。     

黄连解毒汤治疗2型糖尿病

糖尿病是一种严重威胁人们身体健康的常见代谢性疾病,近年来,通过不断研究,认为胰岛素抵抗和胰岛β细胞缺陷与炎症因子和细胞免疫功能的失衡密切相关.黄连解毒汤作为清热解毒的代表方治疗2型糖尿病不仅有丰富的理论基础,而且与现代医学关于2型糖尿病的发病机制也是吻合的.     

胰岛素强化治疗对2型糖尿病大鼠氧化应激的影响研究

目的探讨胰岛素强化治疗对2型糖尿病(T2DM)大鼠氧化应激的影响,为临床胰岛素强化治疗提供理论依据。方法将36只Wistar大鼠随机分为正常对照组(NC组,n=12)和高脂组(HF组,n=24),将HF组大鼠造成T2DM模型后再随机分为2个亚组,即糖尿病对照组(DC组,n=12)和胰岛素治疗组(IT组,n=12)。IT组大鼠皮下注射胰岛素,NC组和DC组大鼠皮下注射等容积0.9%氯化钠溶液,疗程4周,比较3大鼠实验前后血清及肝组织中超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽转移酶(GSM)水平。结果 IT组血清及肝组织中SOD、GSM较DC组升高,差异有统计学意义(P<0.05);DC组较NC组降低,差异有统计学意义(P<0.01);IT组较NC组降低,差异有统计学意义(P<0.05)。IT组血清及肝组织中MDA较DC组降低,差异有统计学意义(P<0.05);DC组较NC升高,差异有统计学意义(P<0.01);IT组较NC组升高,差异有统计学意义(P<0.05)。结论 T2DM大鼠存在脂质过氧化水平升高及抗氧化酶活性下降,胰岛素强化治疗可减轻T2DM大鼠的氧化应激损伤,其机制与改善血脂代谢紊乱,减轻脂毒性有关。     

交泰丸对2型糖尿病大鼠糖脂代谢及肾脏保护作用的实验研究

目的:探讨交泰丸对于2型糖尿病大鼠(T2DM)糖脂代谢及肾脏保护作用。方法:采用尾静脉注射小剂量链脲佐菌素(STZ)同时喂养高脂饮食的方法建立大鼠T2DM模型,将大鼠随机分为模型组、交泰丸组、二甲双胍组、正常对照组,给予相应药物治疗8周,分别称取大鼠体质量以及肾湿重,检测空腹血糖(FPG)、空腹胰岛素(FINS)、血脂(TC、TG、HDL-C、LDLC、NEFA)、血肌酐(Cr)、尿素氮(BUN)、氧化应激相关指标(MDA、SOD、T-AOC)水平,肾脏组织TG含量,计算胰岛素抵抗指数(HOMA-IR),光镜下观察肾脏组织病理变化。结果:与正常组比较,模型组大鼠体质量、肾湿重、空腹血糖(FPG)、空腹胰岛素(FINS)、血脂(TC、TG、LDL-C、NEFA)、血肌酐(Cr)、尿素氮(BUN)、肾脏组织TG含量、MDA水平均升高,HDL-C、SOD、T-AOC水平下降,肾脏组织结构紊乱,可见脂肪沉积;与模型组比较,各治疗组体质量、肾湿重、FPG、FINS、HOMA-IR、血脂(TC、TG、LDL-C、NEFA)、肾脏组织TG含量降低,肾功能及氧化应激相关指标好转,肾脏组织病理学变化改善。结论:交泰丸能够有效改善2型糖尿病大鼠糖脂代谢,并对早期肾脏损害有保护作用,推测其机制可能与改善氧化应激有关。     

红花对2型糖尿病大鼠肾脏氧化应激反应的影响

目的:研究红花对2型糖尿病大鼠肾脏氧化应激反应的影响。方法:采用单侧肾切除加高脂高糖和小剂量链脲佐菌素的方法建立2型糖尿病大鼠模型。分为正常对照、模型和红花低、高剂量组。治疗12周后测定各组生化指标、尿白蛋白排泄率(UAER)和肾皮质超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)活性以及丙二醛(MDA)含量,检测肾皮质P22phox mRNA、P47phox mRNA表达水平。结果:与模型组比较,红花各剂量组血糖水平无显著性差异;血肌酐、尿素氮、UAER水平极显著下降;SOD、GSH-PX活性显著上升;MDA含量极显著下降;P22phox mRNA、P47phox mRNA表达水平显著降低。结论:红花能减轻糖尿病大鼠肾皮质氧化应激反应,有保护肾脏和延缓糖尿病肾病发生的作用。     

黄连解毒汤对2型糖尿病大鼠血清炎性介质和标志物水平的影响

目的:探讨黄连解毒汤对实验性2型糖尿病血清部分炎症介质和标志物的影响,并初步讨论其作用机制.方法:以链脲佐菌素(STZ)静脉注射加高脂肪高热卡饮食饲养建立2型糖尿病大鼠模型,对照观察黄连解毒汤对实验性2型糖尿病大鼠治疗前后口服糖耐量实验(OGTT)、空腹血糖(FBG)、空腹胰岛素(FINS)、白介素1β(IL-1β)、白介素6(IL-6)、肿瘤坏死因子α(TNF-α)、急相反应蛋白C(CRP)一系列指标的影响.结果:给予黄连解毒汤治疗的实验性2型糖尿病大鼠,其血清中FBG、IL-1β、IL-6、TNF-α、CRP的水平比模型对照组明显降低,OGTT显著改善.结论:黄连解毒汤具有降糖、抗炎、改善胰岛素抵抗等作用,其作用机制可能与其改善2型糖尿病的炎症反应程度,改善胰岛素信号传导功能有关.     

体育锻炼、氧化应激、炎症与2型糖尿病

目前随着生活方式的改变和能量的过多摄入,肥胖和2型糖尿病的发病率明显增加。氧化应激和炎症是2型糖尿病的重要发病机制之一。体育锻炼作为一个自然的抗炎和抗氧化剂能够改善胰岛素抵抗,降低2型糖尿病的发病率和病死率。体育锻炼的抗炎和抗氧化机制可能与降低体内CRP、IL-6和TNF-α等炎症因子水平有关。进一步研究体育锻炼的抗炎和抗氧化机制,对预防2型糖尿病的发生、发展具有重要意义。     

酒蒸黄连HPLC指纹图谱及其与不同黄连炮制品的比较研究

目的:建立酒蒸黄连的HPLC指纹图谱,并比较不同黄连炮制品的差异.方法:采用HPLC法测定了酒蒸黄连等不同炮制品样品,运用主成分分析和相似度评价方法分析其结果.结果:建立了酒蒸黄连的HPLC指纹图谱,主成分分析将七批酒蒸黄连样品聚集在一起,并与其它炮制品样品明显分离.结论:酒蒸黄连与姜黄连、萸黄连、酒黄连等炮制品化学成分有一定的差异.本法稳定、准确、重复性好,为酒蒸黄连的质量标准研究提供了科学依据.     

黄连素对 2型糖尿病大鼠肾脏的保护作用

目的:观察黄连素对2型糖尿病大鼠肾脏的保护作用。方法:采用STZ诱导2型糖尿病大鼠模型,给予黄连素0.1g/kg·d治疗12周,检测各组血糖、胰岛素、血脂、肾皮质丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性,并观察尿白蛋白排泄量及肾组织病理改变。结果:与糖尿病组相比,黄连素治疗组血糖、胰岛素、TG、TC、LDL-c均下降,而HDL-c升高;肾皮质SOD活性明显升高,MDA含量显著下降;尿白蛋白排泄量明显减少,肾脏组织病理改变明显减轻。结论:黄连素可以明显改善2型糖尿病大鼠的肾脏损害,延缓糖尿病肾脏病变的发生和发展。     

探究盐酸二甲双胍肠溶胶囊对2型糖尿病周围神经病变患者的氧化应激作用

目的探究盐酸二甲双胍肠溶胶囊对2型糖尿病周围神经病变患者的氧化应激作用。方法 84例2型糖尿病周围神经病变患者,依据随机数字表法分为研究组和对照组,各42例。对照组患者给予那格列奈片治疗,研究组患者给予盐酸二甲双胍肠溶胶囊治疗。比较两组临床疗效。结果治疗后,研究组患者腓总神经及正中神经感觉传导速度(SNCV)及运动传导速度(MNCV)均显著高于治疗前(P<0.05),且显著高于对照组(P<0.05),血清丙二醛(MDA)水平显著低于对照组(P<0.05),超氧化物歧化酶(SOD)活性显著高于对照组(P<0.05)。结论盐酸二甲双胍肠溶胶囊能够有效抑制2型糖尿病周围神经病变患者的氧化应激反应,并显著提高患者的神经传导速度,值得临床推广。     

2型糖尿病大鼠主动脉内皮细胞氧化损伤及缬沙坦的保护作用

目的探讨2型糖尿病大鼠氧化应激与主动脉内皮细胞损伤的关系,观察缬沙坦对两者的影响。方法SD大鼠,用长期高能量饮食加小剂量注射链脲佐菌素(STZ)的方法复制模型。注射STZ12wk末,将大鼠分为3组:正常组、糖尿病组、缬沙坦治疗组(24mg·kg-1·d-1,灌胃给药8wk)。在注射STZ12和20wk末,检测大鼠的内皮依赖性血管舒张反应及主动脉内皮形态,血清超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性,丙二醛(MDA)和一氧化氮(NO)含量,以及主动脉一氧化氮合酶(NOS)基因表达情况。结果①12wk末,糖尿病大鼠主动脉对低浓度乙酰胆碱(ACh)舒张反应减弱,局部内皮隆起,血清SOD、GSH-Px活性增强,MDA和NO含量增加,主动脉iNOS mRNA表达明显上调,eNOS mRNA表达无明显改变。②20wk末,糖尿病大鼠主动脉对各浓度ACh的反应性均减弱,主动脉内皮变性、坏死,血清SOD、GSH-Px活性减弱,MDA含量进一步增加,NO含量下降,主动脉iNOS mRNA表达仍升高,eNOS mRNA表达降低,缬沙坦治疗后能减轻主动脉病变,改善血清SOD、GSH-Px、MDA、NO及主动脉NOS mRNA表达的异常。结论糖尿病大鼠的氧化应激和NO系统的紊乱参与了主动脉病变过程,增强机体抗氧化能力及调节NO生成可能是缬沙坦发挥主动脉保护作用的机制之一。     

缬沙坦对2型糖尿病大鼠心肌病变的防治作用

目的　观察 2型糖尿病大鼠心肌病变时一氧化氮(NO)、一氧化氮合酶 (NOS)基因表达的变化及缬沙坦对心肌病变的防治作用。方法　采用高能量饮食加小剂量腹腔注射链脲佐菌素 (STZ)的方法 ,建立 2型糖尿病大鼠模型。缬沙坦连续灌胃 8wk。观察注射STZ 12wk和 2 0wk后大鼠的心功能、心脏重量指数、心肌和血浆中NO含量、心肌中eNOSmRNA和iNOSmRNA表达情况。结果　从注射STZ后的 12wk到 2 0wk ,2型糖尿病组大鼠左心室收缩和舒张功能进行性减退 ,心脏重量指数增加 ;心肌和血浆中NO水平于注射STZ 12wk时上升 ,2 0wk时下降 ;心肌iNOSmR NA的表达在 12wk和 2 0wk时均明显增加 ,eNOSmRNA的表达在 12wk时无明显改变 ,在 2 0wk时则明显减少 ;缬沙坦能使上述异常显著减轻。结论　NO及NOSmRNA基因表达的异常改变可能参与了 2型糖尿病心肌病变发生发展的过程 ;缬沙坦对 2型糖尿病心肌病具有一定防治作用。     

The protective effect of taurine against cyclosporine A-induced oxidative stress and hepatotoxicity in rats

Cyclosporine A (CsA) is the immunosuppressor which is most frequently used in transplant surgery and in the treatment of autoimmune diseases. Oxidative stress has been implicated as one of the possible mechanisms of CsA-induced hepatotoxicity. The present investigation examined the ability of taurine as an antioxidant to protect against CsA-induced oxidative stress and hepatotoxicity. CsA hepatotoxicity was induced by subcutaneous injection of CsA at a dose of 20mg/kg body weight daily for 21 days. Hepatotoxicity was assessed by reduced serum total protein level and increased serum levels of gamma glutamyl transferase (GGT), alanine aminotransferase (ALT), and aspartate aminotransaminase (AST). CsA treatment increased lipid peroxidation measured as thiobarbituric acid reactive substances (TBARS) concentration and decreased reduced glutathione (GSH) content and activities of catalase and glutathione peroxidase (GSH-Px) in the rat liver. Taurine administration (1% in the drinking water) for 3 days before and concurrently during CsA injections improved liver functions, as indicated by decline of serum transaminases and GGT levels and elevation of serum total protein. Moreover, taurine significantly reduced hepatic TBARS and increased GSH content and catalase and GSH-Px activities in the hepatic tissue. These results indicate that taurine has a protective action against CsA hepatotoxicity and suggest that taurine may find clinical application against a variety of toxins where cellular damage is a consequence of reactive oxygen species.     

The protective effect of flavonol quercetin against ultraviolet a induced oxidative stress in rats

Ultraviolet A (UVA) light exposed cells can induce the production of reactive oxygen species (ROS) which can damage the cellular elements. Antioxidants can interfere with the production of ROS. In this study, malondialdehyde (MDA), reduced glutathione (GSH), glutathione reductase (GSSGR), glutathione peroxidase (GPx), catalase (CAT) and superoxide dismutase (SOD) levels were measured in the liver of rats exposed to UVA light in various doses. The effects of quercetin were determined as antioxidant on those parameters. Rats were divided into three groups as control, ultraviolet (UV), and ultraviolet+quercetin (UV+Q). UV and UV+Q group rats were irradiated 4 h per day with UVA light (1.25 mW/cm(2)) during periods of 0,3,6,9 days. Thus, on days 0,3,6 and 9, the rats have received 0,54,108,162 W/cm(2) light, respectively. Quercetin (50 mg/kg body wt.) was administered intraperitoneally before each irradiation period in the UV+Q group rats. MDA level in the UV group increased significantly on day-9 when compared to the control group (P<0.05). The MDA levels in the UV+Q group decreased significantly on day-6 and 9 in comparison with the UV group (P<0.05, P<0.001, respectively). GSH levels in all groups were not significantly different. GSSGR and GPx activities in the UV group were significantly lower on day-6 and 9 than in the control group (P<0.001). On all days these enzyme activities in the UV+Q group were significantly higher than in the UV group and higher than in the control group (P<0.001). SOD and CAT activities in the UV group decreased significantly on day-3, 6, and 9 in comparison with the control group (P<0.001). These enzyme activities also increased significantly in the UV+Q group on all days when compared to the UV group (P<0.001). This study demonstrated that the exposure of rats to UVA led to oxidative stress as reflected by increased MDA levels and reduced enzymic antioxidant levels, quercetin may be useful by reducing or preventing photobiologic damage.     

Induction of oxidative stress by endosulfan and protective effect of lipid-soluble antioxidants against endosulfan-induced oxidative damage

The toxic mechanism of endosulfan, a widely used organochlorine pesticide, was investigated in Saccharomyces cerevisiae and human cell lines. A concentration-dependent inhibition of cell growth was observed when S. cerevisiae was exposed to endosulfan, and its cytotoxicity (IC(50)) was found to be 49 microM and 86 microM in HepG2 and HeLa human cell lines, respectively. The treatment of S. cerevisiae with endosulfan resulted in oxidative damage, as demonstrated by thiobarbituric acid-reactive substance (TBARS) production, in a dose-dependent manner, and the growth inhibition was recovered by treatment with lipid-soluble antioxidants, such as alpha-tocopherol or beta-carotene, suggesting that endosulfan toxicity may be closely associated with endosulfan-induced reactive oxygen species (ROS) generation. The inhibition of cellular respiration by endosulfan treatment and the recovery of respiration activity by antioxidant treatment confirmed that endosulfan induces oxidative stress and inhibits respiration via ROS generation. These results suggest that unicellular yeast might provide a useful system for elucidating the toxicity of endosulfan.     

2型糖尿病微血管并发症与DNA氧化损伤的关系

目的 探讨2型糖尿病(T2DM)合并微血管并发症患者的DNA氧化损伤.方法 将87例T2DM患者分为糖尿病微血管并发症(A)组(n=56)和T2DM无微血管并发症(B)组(n=31),另选65例正常体检者为正常对照(C)组.用ELISA方法测定血液单核细胞DNA氧化损伤指标-8羟基脱氧鸟嘌呤(8-OHdG)水平.结果 A、B组血液8-OHdG水平均较C组显著升高;A组病程、24 h尿白蛋白、血液8-OHdG水平也较B组显著升高.结论 T2DM合并微血管并发症患者的DNA氧化损伤较正常对照及无并发症糖尿病患者明显,对糖尿病合并微血管并发症者施行抗氧化治疗是合理的.     

Di(2-ethylhexyl)phthalate-induced renal oxidative stress in rats and protective effect of selenium

This study was designed to examine the oxidative stress potential of di(2-ethylhexyl)phthalate (DEHP) on rat kidney and to evaluate possible protective effect of selenium (Se) status. Se deficiency (SeD) was produced in 3-week old Sprague-Dawley rats by feeding them ≤ 0.05 Se mg/kg diet for 5 weeks; Se supplementation group (SeS) was on 1 mg Se/kg diet. DEHP treated groups received 1000 mg/kg dose by gavage during the last 10 days of the feeding period. Activities of antioxidant selenoenzymes [glutathione peroxidase 1 (GPx1), glutathione peroxidase 4 (GPx4), thioredoxin reductase (TrxR)], catalase (CAT), superoxide dismutase (SOD), and glutathione S-transferase (GST); concentrations of total glutathione (GSH), thiols and thiobarbituric acid reactive substance (TBARS) levels were measured. DEHP treatment was found to induce oxidative stress in rat kidney, as evidenced by significant decreases in GPx1 (~20%) and SOD (~30%) activities and GSH levels (~20%), along with marked decrease in thiol content (~40%) and increase in TBARS (~30%) levels. The effects of DEHP was more pronounced in SeD rats, whereas Se supplementation was protective by providing substantial elevations of GPx1 and GPx4 activities and GSH levels. These findings emphasized the critical role of Se as an effective redox regulator and the importance of Se status in protecting renal tissue from the oxidant stressor activity of DEHP.     

Di(2-ethylhexyl)phthalate-induced renal oxidative stress in rats and protective effect of selenium

This study was designed to examine the oxidative stress potential of di(2-ethylhexyl)phthalate (DEHP) on rat kidney and to evaluate possible protective effect of selenium (Se) status. Se deficiency (SeD) was produced in 3-week old Sprague?Dawley rats by feeding them ≤ 0.05 Se mg/kg diet for 5 weeks; Se supplementation group (SeS) was on 1 mg Se/kg diet. DEHP treated groups received 1000 mg/kg dose by gavage during the last 10 days of the feeding period. Activities of antioxidant selenoenzymes [glutathione peroxidase 1 (GPx1), glutathione peroxidase 4 (GPx4), thioredoxin reductase (TrxR)], catalase (CAT), superoxide dismutase (SOD), and glutathione S-transferase (GST); concentrations of total glutathione (GSH), thiols and thiobarbituric acid reactive substance (TBARS) levels were measured. DEHP treatment was found to induce oxidative stress in rat kidney, as evidenced by significant decreases in GPx1 (~20%) and SOD (~30%) activities and GSH levels (~20%), along with marked decrease in thiol content (~40%) and increase in TBARS (~30%) levels. The effects of DEHP was more pronounced in SeD rats, whereas Se supplementation was protective by providing substantial elevations of GPx1 and GPx4 activities and GSH levels. These findings emphasized the critical role of Se as an effective redox regulator and the importance of Se status in protecting renal tissue from the oxidant stressor activity of DEHP.     

Clinacanthus nutans attenuates atherosclerosis progression in rats with type 2 diabetes by reducing vascular oxidative stress and inflammation

ContextAtherosclerosis predisposes individuals to adverse cardiovascular events. Clinacanthus nutans L. (Acanthaceae) is a traditional remedy used for diabetes and inflammatory conditions.ObjectivesTo investigate the anti-atherosclerotic activity of a C. nutans leaf methanol extract (CNME) in a type 2 diabetic (T2D) rat model induced by a high-fat diet (HFD) and low-dose streptozotocin.Materials and methodsSixty male Sprague-Dawley rats were divided into five groups: non-diabetic fed a standard diet (C), C + CNME (500 mg/kg, orally), diabetic fed an HFD (DM), DM + CNME (500 mg/kg), and DM + Metformin (DM + Met; 300 mg/kg). Treatment with oral CNME and metformin was administered for 4 weeks. Fasting blood glucose (FBG), serum lipid profile, atherogenic index (AI), aortic tissue superoxide dismutase levels (SOD), malondialdehyde (MDA), and tumour necrosis factor-alpha (TNF-α) were measured. The rats’ aortas were stained for histological analysis and intima-media thickness (IMT), a marker of subclinical atherosclerosis.ResultsThe CNME-treated diabetic rats had reduced serum total cholesterol (43.74%; p = 0.0031), triglycerides (80.91%; p = 0.0003), low-density lipoprotein cholesterol (56.64%; p = 0.0008), AI (51.32%; p < 0.0001), MDA (60.74%; p = 0.0026), TNF-α (61.78%; p = 0.0002), and IMT (39.35%; p < 0.0001) compared to untreated diabetic rats. SOD level, however, increased (53.36%; p = 0.0326). These CNME effects were comparable to those in the metformin-treated diabetic rats.ConclusionsC. nutans possesses anti-atherosclerotic properties, which may be due to reductions in vascular tissue oxidative stress, inflammation, and serum AI. Continued studies on atherosclerotic animal models are suggested.     

DJ-1保护多巴胺能神经元抵抗过氧化氢氧化应激损伤的研究

目的 探讨DJ-1保护多巴胺能神经元免受过氧化氢(H₂O₂)损伤的机制。 方法 使用神经生长因子(NGF)将大鼠嗜铬细胞瘤细胞(PC12细胞)诱导为多巴胺能神经元模型。H₂O₂处理引起细胞氧化应激损伤模型,CCK-8试剂盒检测细胞活性,DHE染色检测细胞内ROS水平。PI / Hoechst染色检测细胞凋亡,蛋白质免疫印迹法(Western blot)检测DJ-1和TH蛋白的表达。构建DJ-1过表达载体,检测DJ-1对H₂O₂中PC12细胞的保护作用及对细胞内活性氧(ROS)的影响。RT-qPCR检测α-synuclein,p53,Bax,Bcl-2的表达变化。 结果 H₂O₂处理可显着降低PC12细胞的活性,H₂O₂处理24 h以上可引起细胞凋亡。H₂O₂处理下调DJ-1蛋白和TH蛋白的表达,并且在RNA水平上α-突触核蛋白的表达增加。另外 p53, Bax和 caspase-3表达增加, Bcl-2表达减少。DJ-1的过表达可以抑制H₂O₂引起的ROS增加,DJ-1可以维持细胞活性,减少H₂O₂的凋亡。在RNA水平抑制α-突触核蛋白,p53,bax,bcl-2的凋亡和抗凋亡基因表达变化。 结论 DJ-1能够抑制H₂O₂引起的 ROS水平升高,减少α-synuclein积累,抑制 p53,凋亡基因如 bax的表达减弱了多巴胺能神经元中H₂O₂诱导的氧化应激损伤。