依达拉奉对大鼠实验性自身免疫性脑脊髓炎的保护作用

目的:研究依达拉奉对实验性自身免疫性脑脊髓炎(Experimental Autoimmune Encephalomyelitis,EAE)的影响。方法:72只健康成年雌性Wistar大鼠随机分为:正常对照组、EAE组、EAE+小剂量依达拉奉组、EAE+大剂量依达拉奉组(n=18)。正常对照组注射生理盐水,其它组采用自制完全抗原诱导EAE模型。EAE组建模后不做任何处理,EAE+小剂量依达拉奉组、EAE+大剂量依达拉奉组分别在建模后给予依达拉奉4mg/k·d、10mg/k·d。比较各组发病率并行神经功能评分,取脊髓组织行HE染色、iNOS、OPN免疫组织化学染色观察。结果:依达拉奉干预组大鼠较EAE组发病率、神经功能缺损评分均明显降低(P<0.05)。HE结果显示依达拉奉干预组较EAE组炎症反应减少,损伤程度减轻。依达拉奉组iNOS、OPN表达均明显小于EAE组(P<0.05)。大剂量依达拉奉iNOS、OPN表达均低于小剂量依达拉奉组(P<0.05)。结论:依达拉奉对EAE具有保护作用,可能与抑制小神经胶质细胞活化,减轻炎症反应,降低iNOS和OPN表达有关。     

依达拉奉对大鼠实验性自身免疫性脑脊髓炎的保护作用

目的：研究依达拉奉对实验性自身免疫性脑脊髓炎（Experimental Autoimmune Encephalomyelitis,EAE）的影响。方法：72只健康成年雌性Wistar大鼠随机分为：正常对照组、EAE组、EAE＋小剂量依达拉奉组、EAE＋大剂量依达拉奉组（n=18）。正常对照组注射生理盐水,其它组采用自制完全抗原诱导EAE模型。EAE组建模后不做任何处理,EAE＋小剂量依达拉奉组、EAE＋大剂量依达拉奉组分别在建模后给予依达拉奉4mg/k·d、10mg/k·d。比较各组发病率并行神经功能评分,取脊髓组织行HE染色、iNOS、OPN免疫组织化学染色观察。结果：依达拉奉干预组大鼠较EAE组发病率、神经功能缺损评分均明显降低（P〈0.05）。HE结果显示依达拉奉干预组较EAE组炎症反应减少,损伤程度减轻。依达拉奉组iNOS、OPN表达均明显小于EAE组（P〈0.05）。大剂量依达拉奉iNOS、OPN表达均低于小剂量依达拉奉组（P〈0.05）。结论：依达拉奉对EAE具有保护作用,可能与抑制小神经胶质细胞活化,减轻炎症反应,降低iNOS和OPN表达有关。     

依达拉奉通过JNK对大鼠离体心肌缺血再灌注损伤的保护作用

目的:研究依达拉奉(Edaravone)对大鼠离体心肌缺血再灌注损伤的保护作用.方法:将54只SD大鼠随机分为3组,包括对照组(control group),缺血再灌注组(I/R group),依达拉奉组(Ed group).灌注液为K-H液,37℃下建立心肌缺血再灌注模型,预灌注15min,缺血30min,再灌注40 min,分别测量①复灌20和40min时心功能指标:心率(HR)、左室收缩压(LVDP)、左室舒张末压(LVEDP)、心室内压最大变化速率(±dp/dtmax),②复灌20和40 min时肌酸激酶(CK)和乳酸脱氢酶(LDH)活性,③复灌40 min时超氧化物歧化酶(SOD)活性和和丙二醛(MDA)浓度,④复灌40min时心肌梗死面积,⑤复灌40min时心肌组织中JNK的磷酸化水平.结果:①依达拉奉组的±dp/dtmax明显回升(P<0.05),同时LVEDP、LVDP等指标也有明显改善(P<0.05);②再灌注40min时,与缺血再灌注组比,依达拉奉明显降低LDH和CK;③依达拉奉能显著降低MDA浓度,同时提高SOD水平(P<0.05);④依达拉奉组心肌梗死面积小于缺血再灌注组(P<0.05);⑤依达拉奉降低缺血心肌组织中磷酸化JNK的水平(P<0.05).结论:依达拉奉可以改善缺血心肌的血流动力学,增加心肌收缩力,减少心肌梗死面积;能发挥清除氧自由基,扭转氧化与抗氧化平衡系统失调的作用;其对离体心肌缺血再灌注的保护作用可能与JNK途径密切相关.     

依达拉奉对小鼠肺型氧中毒的保护作用及其机制

目的:探讨依达拉奉(edaravone)对肺型氧中毒的保护作用及其机制。方法:30只C57BL/6雄性小鼠,随机分成3组(n=10):空气对照组、高压氧暴露组及依达拉奉预防组,干预组腹腔注射依达拉5 mg/(kg·d), 连续3 d后,暴露于2.3 ATA,≥95% 氧气中6 h,出舱后收集肺组织,检测肺湿干比。肺组织经苏木素-伊红染色后行病理分析。ELISA检测肺组织中细胞因子、抗氧化酶表达变化。Western检测凋亡基因。结果:依达拉奉注射后可明显减轻高压氧导致的肺损伤,降低肺湿干比,减少细胞因子IL-1β及凋亡蛋白cleaved-caspase3的表达,但对抗氧化酶无明显影响。结论:依达拉奉预防性应用可通过减轻炎症及凋亡对肺型氧中毒起到保护作用。     

依达拉奉对MPP+处理的PC12细胞线粒体融合和分裂平衡的保护作用

本文旨在探讨依达拉奉(edaravone, Eda)对帕金森病细胞模型线粒体融合、分裂动态平衡的作用及机制。用500μmol/L1-甲基-4-苯基吡啶离子(1-methyl-4-phenylpyridinium, MPP^+)处理PC12细胞建立帕金森病细胞模型,采用噻唑蓝(MTT)比色法检测不同浓度Eda对MPP^+处理的PC12细胞存活率的影响,用激光共聚焦显微镜检测线粒体形态,用Western blot检测线粒体融合与分裂相关蛋白OPA1、MFN2、DRP1和Fis1的表达变化。结果显示,预先加入不同浓度的Eda能减轻MPP^+处理的PC12细胞损伤,作用呈一定的量效关系;经MPP^+处理48 h,PC12细胞线粒体出现碎片化,OPA1和MFN2蛋白表达下调,DRP1和Fis1蛋白表达上调,而Eda预处理能逆转PC12细胞的上述变化,但对Fis1的蛋白表达没有影响。以上结果提示,Eda可上调OPA1和MFN2的蛋白表达,下调DRP1的表达,从而抑制线粒体碎片化,发挥神经细胞线粒体保护作用。     

奥拉西坦联合依达拉奉对急性脑梗死的疗效评价

目的:探讨奥拉西坦联合依达拉奉对急性脑梗死的疗效以及安全性.方法:对我院收治的132例急性脑梗死患者随机分为实验组以及对照组,实验组患者采用奥拉西坦联合依达拉奉进行治疗,对照组患者采用依达拉奉进行治疗,对两组患者治疗前后NIHSS评分、Barthel指数、临床疗效以及脑梗死面积进行比较.结果:实验组患者在接受治疗2周期NIHSS评分、Barthel指数明显优于对照组(P＜0.05);实验组患者其治疗痊愈以及显效例数为55例以及9例明显优于对照组的8例以及8例(P＜0.05);实验组患者接受治疗后其梗死面积为7.21± 4.32cm2,明显优于对照组的14.32± 5.49 cm2.结论:对于急性脑梗死患者采用奥拉西坦联合依达拉奉进行治疗,可有效改善患者预后,降低伤残率,改善患者预后.     

依达拉奉对犬自体肾移植缺血再灌注损伤的保护作用研究

目的:探讨依达拉奉对犬自体肾移植缺血再灌注损伤的影响及机制。方法:将18只体重匹配的健康杂种犬随机分为假手术组(S组)、依达拉奉组(ED组)、生理盐水组(PS组),每组各6只。S组仅进行肾手术切除;ED组在阻断前在供体静脉内注入依达拉奉10 mg/kg,然后使用200 mL加入依达拉奉10 mg/kg的UW液灌洗供体肾并在同样的保存液中保存供体肾8小时,且再灌注开始时立即在受体静脉内给予依达拉奉10 mg/kg;PS组同法使用相同体积的生理盐水。再灌注4 h后检测MDA、MPO、SOD、iNOS、eNOS等活性;术后24 h检测血清肌酐(Cr)、尿素氮(BUN)浓度;光镜下观察肾组织病理学改变。结果:PS组MDA显著高于S组及ED组(P0.05),PS组MPO含量亦低于S组及ED组(P0.05)。PS组SOD、eNOS含量显著低于于S组及ED组(P0.05),PS组iNOS含量高于S组及ED组(P0.05),ED组的肾损伤明显减轻。结论:依达拉奉能减轻肾移植缺血再灌注损伤,其机制可能与减轻肾脂质过氧化反应有关。     

依达拉奉对犬自体肾移植缺血再灌注损伤的保护作用研究

目的：探讨依达拉奉对犬自体肾移植缺血再灌注损伤的影响及机制。方法：将18 只体重匹配的健康杂种犬随机分为假手术组（S组）、依达拉奉组（ED组）、生理盐水组（PS 组）,每组各6只。S 组仅进行肾手术切除;ED组在阻断前在供体静脉内注入依达拉奉10 mg/kg,然后使用200 mL加入依达拉奉10 mg/kg 的UW液灌洗供体肾并在同样的保存液中保存供体肾8 小时,且再灌注开始时立即在受体静脉内给予依达拉奉10 mg/kg;PS 组同法使用相同体积的生理盐水。再灌注4 h 后检测MDA、MPO、SOD、iNOS、eNOS等活性;术后24 h 检测血清肌酐（Cr）、尿素氮（BUN）浓度;光镜下观察肾组织病理学改变。结果：PS 组MDA显著高于S 组及ED组（P〈0.05）,PS组MPO 含量亦低于S 组及ED组（P〈0.05）。PS组SOD、eNOS 含量显著低于于S组及ED组（P〈0.05）,PS 组iNOS含量高于S 组及ED 组（P〈0.05）,ED组的肾损伤明显减轻。结论：依达拉奉能减轻肾移植缺血再灌注损伤,其机制可能与减轻肾脂质过氧化反应有关。     

长春西汀联合依达拉奉治疗急性脑梗死的临床价值分析

目的:观察长春西汀联合依达拉奉治疗急性脑梗死的临床疗效。方法:选取我院确诊的急性脑梗死96例患者随机分组,依达拉奉组给予单纯依达拉奉注射液治疗,联合组采用依达拉奉和长春西汀联合使用,疗程14天。结果:依达拉奉组与联合治疗组神经功能总有效率相当(67.39%vs.72.00%,p0.05)。进一步分析联合治疗组神经功能显效率高于依达拉奉组(38.00%vs.23.91%,p0.05)。神经功能缺损评分和日常活动能力评分显示,依达拉奉和长春西汀联合治疗更有优势。结论:长春西汀联合依达拉奉治疗急性脑梗死具有良好的临床应用价值。     

针刺联合依达拉奉对缺血再灌注大鼠视网膜自由基代谢的影响

目的:研究针刺联合依达拉奉对大鼠视网膜缺血再灌注时自由基代谢的影响.方法:大鼠随机分为五组:假手术组、模型组、针刺组、依达拉奉组和联合(针刺+依达拉奉)组.建立缺血再灌注模型,于造模后1d,行视网膜电流图(ERG)检查,取视网膜组织,测定各组MDA含量及T-SOD、GSH-Px、CAT活性的变化.结果:①ERG a、b波振幅相对恢复率:联合组、针刺组及依达拉奉组与模型组相比,a、b波振幅相对恢复率升高,差异有显著性(P＜0.05),与针刺组和依达拉奉组相比,联合组作用更为显著(P＜0.05).②MDA含量及T-SOD、GSH-Px、CAT活性:联合组、针刺组及依达拉奉组与模型组相比,MDA显著降低,SOD、GSH-Px、CAT显著升高,差异有显著性(P＜0.05),联合组作用显著优于针剌组或依达拉奉组(P＜0.05).结论:针刺联合依达拉奉具有干预自由基代谢作用,明显减轻缺血再灌注引起的视网膜氧化应激损伤,对视网膜功能起保护作用.     

The therapeutic effects of edaravone on collagen-induced arthritis in rats

Current research suggests that synovial phagocytic cells remove excessive amounts of free oxygen radicals (reactive oxygen species [ROS]), thereby preventing damage to synovial tissues. Moreover, ROS may affect the expression of growth arrest and DNA damage inducible α (GADD45A), thus further promoting the activation of synovial fibroblasts. Male adult rats were assessed for progression of collagen-induced arthritis (CIA) using a macroscopic arthritis scoring system of the hind paws and by measuring the changes in the rat's body weight, and activity level before and after diagnosis of CIA. Rats were intraperitoneally injected twice daily with edaravone at doses of 3, 6, and 9 mL/kg. Samples were taken at 2, 4, and 6 weeks, respectively. Edaravone was found to significantly reduce macroscopic arthritis and microscopic pathology scores in CIA rats. The concentration of endothelial nitric oxide synthase-6, glutathione, and heme oxygenase-1 in the serum of rats decreased, as was the production of ROS around the synovium and inflammatory factors. Moreover, ROS-1 increased the expression of the nuclear factor-κB (NF-κB) p65 protein by altering the expression level of GADD45A, causing aggravation of tissue damage. Edaravone also significantly improved the physiological condition of CIA rats, including appetite, weight changes, and loss of fur, as well as limb mobility. We believe that edaravone acts to reduce the expression of NF-ĸB p65 by clearing ROS, which causes reduced expression of GADD45A, and subsequently reduces the level of apoptosis and inflammatory response proteins, thereby reducing the symptoms of CIA. We, therefore, propose that edaravone is an effective option for clinical treatment of rheumatic arthritis.     

Cadmium induced Drp1-dependent mitochondrial fragmentation by disturbing calcium homeostasis in its hepatotoxicity

Mitochondria are critical targets in the hepatotoxicity of cadmium (Cd). Abnormal mitochondrial dynamics have been increasingly implicated in mitochondrial dysfunction in pathophysiological conditions. Therefore, our study aimed to investigate the effects and underlying mechanism of Cd on mitochondrial dynamics during hepatotoxicity. In the L02 liver cell lines, 12 μM cadmium chloride (CdCl₂) exposure induced excessive mitochondrial fragmentation as early as 3 h post-treatment with Cd, which preceded the mitochondrial dysfunction such as reactive oxygen species (ROS) overproduction, mitochondrial membrane potential (ΔΨm) loss and ATP reduction. Concurrent to mitochondrial fragmentation, CdCl₂ treatment increased the protein levels of dynamin-related protein (Drp1) and promoted the recruitment of Drp1 into mitochondria. Strikingly, mitochondrial fragmentation also occurred in the liver tissue of rats exposed to CdCl₂, accompanied by enhanced recruitment of Drp1 into mitochondria. Moreover, in L02 cells, Drp1 silencing could effectively reverse Cd-induced mitochondrial fragmentation and mitochondrial dysfunction. Furthermore, the increased expression and mitochondrial recruitment of Drp1 were tightly related to the disturbance of calcium homeostasis, which could be prevented by both chelating [Ca²⁺]_i and inhibiting [Ca²⁺]_m uptake. Overall, our study indicated that Cd induced Drp1-dependent mitochondrial fragmentation by disturbing calcium homeostasis to promote hepatotoxicity. Manipulation of Drp1 may be the potential avenue for developing novel strategies to protect against cadmium-induced hepatotoxicity.     

清脑方对缺血性眩晕大鼠脑损伤的保护作用

目的 初步研究清脑方（Qingnaofang,QNF）对缺血性眩晕大鼠脑损伤的保护作用及其作用机制.方法 采用手术结扎右侧颈总动脉和锁骨下动脉致大鼠右侧半脑不完全脑缺血建立缺血性眩晕大鼠模型.分为模型组,QNF 1.04、0.52、0.26 g/kg组,盐酸地芬尼多15 mg/kg组,银杏叶片5.76 mg/kg组以及假手术组,观察QNF对旋转刺激缺血性眩晕大鼠跳台逃避潜伏期的影响,取材并测定动物缺血侧组织Lac、LDH、SOD、MDA、NO及NOS的含量或活性.结果 （1）与模型组相比,QNF 1.04、0.52、0.26 g/kg组大鼠跳台逃避电击潜伏期分别缩短53.6%（P〈0.01）、33.8%（P〈0.05）、56.5%（P〈0.01）.（2）QNF 1.04、0.52、0.26 g/kg均可显著降低缺血侧脑组织中Lac的含量以及LDH的活力 （P〈0.05,P〈0.01）,降低其TNOS及iNOS活力 （P〈0.01）;QNF 0.52 g/kg剂量能够明显降低缺血侧脑组织中SOD活力;QNF 0.52、0.26 g/kg剂量可显著降低其MDA和NO的含量 （P〈0.05,P〈0.01）.结论 QNF对缺血性眩晕大鼠脑损伤有一定的保护作用,能够减轻模型动物的眩晕症状,其脑保护作用机制可能与改善缺血脑组织能量代谢,减少氧化应激和炎性损伤有关.     

小檗碱对大鼠脑缺血/再灌注损伤的保护作用及免疫机制

目的:探讨小檗碱对大鼠脑缺血/再灌注损伤的保护作用及免疫机制。方法:50只SD大鼠随机分为假手术组(Sham group)、模型组(Model group)、小檗碱低剂量组(BBR-L,25 mg/kg)、小檗碱中剂量组(BBR-M,50 mg/kg)、小檗碱高剂量组(BBR-H,100 mg/kg),每组各10只。采用Longa线栓法建立脑缺血/再灌注大鼠模型,缺血2h后再灌注24 h处理。于造模成功2 h后灌胃给药,假手术组和模型组组按上述方法同体积给予生理盐水。给药24 h后,测定各组大鼠神经功能缺损程度评分及脑梗死率;采用ELISA法检测抗氧化酶SOD和GSH-Px的活性、细胞因子TNF-α、IFN-β、IL-6和NO的含量;采用流式细胞术检测CD4⁺、CD8⁺及CD4⁺/CD8⁺血清含量;进一步采用RT-qPCR与Western blot技术检测大鼠脑组织内NF-κB-NLRP3信号轴关键基因及蛋白的表达情况。结果:与假手术组比较,模型组大鼠神经功能缺损程度、脑梗死率均升高(P<0....     

筒鞘蛇菰提取物蛇菰多糖对D-半乳糖诱导大鼠肝损伤的保护作用及其机制

目的:探讨筒鞘蛇菰提取物蛇菰多糖(BIH)对D-半乳糖(D-gal)致大鼠肝损伤的保护作用及机制.方法:雄性SD大鼠60只,随机分为正常组(Con)、模型组(D-gal)、蛇菰多糖低剂量组(D-gal+50 mg/kg BIH,BIH-L)、蛇菰多糖中剂量组(D-gal+100 mg/kg BIH,BIH-M)、蛇菰多...     

脂氧素受体激动剂BML-111对大鼠急性肝损伤的干预作用及其机制*

目的: 探索脂氧素对急性肝损伤的作用及机制。方法: SD大鼠24只随机分为4组(n=6):正常对照组:皮下注射橄榄油,剂量1.8 ml/kg。模型组:皮下注射40%四氯化碳(CCL4)油剂(橄榄油为溶剂),剂量3 ml/kg。BML-111治疗组:皮下注射Lipoxin受体激动剂BML-111,剂量1 mg/kg,30 min后处理同模型组。BOC-2阻断剂组:皮下注射Lipoxin受体阻断剂BOC-2,剂量50 μg/kg,30 min后处理同BML-111组。HE染色观察肝组织病理学变化,判断肝损伤情况。血清学检测血清谷丙转氨酶(ALT)及谷草转氨酶(AST)活性;试剂盒法检测大鼠肝组织中髓过氧化物酶(MPO)活性;ELISA法测定血清中血管紧张素转化酶(ACE)、血管紧张素转化酶2(ACE2)、血管紧张素II(AngII)、血管紧张素1-7(Ang-(1-7))的含量。Western blot检测肝组织中Ang II、Ang-(1-7)的蛋白含量。结果: 治疗组较模型组和阻断剂组的肝损伤程度减轻;BML-111降低CCL4损伤的大鼠血清中ACE、AngII的含量(P＜0.01)及升高血清中ACE2、Ang-(1-7)的含量(P＜0.01)。BML-111增加肝组织中Ang-(1-7)含量,降低CCL4损伤的大鼠组织中AngII含量。结论: 结果表明脂氧素受体激动剂BML-111对大鼠急性肝损伤的干预作用及其机制,可能与调节AngII和Ang-(1-7)有关。     

醒脑静对颅脑创伤的保护作用

目的：探讨醒脑静对颅脑损伤大鼠的保护作用及其机制。方法：健康雄性成年SD大鼠63只,随机分为3组（n=21）：假手术组、模型组、醒脑静组。模型组与醒脑静组均采用自由落体撞击伤方法制作创伤性脑损伤模型,假手术组仅行开颅术,不造成脑损伤。醒脑静组盆大鼠造模后10min内经尾静脉注射醒脑静注射液10ml／（kg·d）,模型组与假手术组则经尾静脉注射等量0．9％氯化钠溶液,三组均连续给药7d。给药第7天比较各组大鼠血清中S-100B蛋白和神经特异性烯醇化酶（NSE）水平,脑组织含水量,检测血清中超氧化物歧化酶（SOD）、丙二醛（MDA）和谷胱甘肽过氧化物酶（GSH—Px）含量,并对各组大鼠进行神经功能缺损评分。结果：与假手术组比较,醒脑静组和模型组均有明显的神经缺损,脑组织含水量、MDA、S-100B蛋白和NSE水平明显升高,SOD、GSH-Px含量明显降低;醒脑静组与模型组比较,醒脑静组神经缺损程度及脑含水量显著低于模型组,血清中MDA和NSE水平明显低于模型组,SOD、GSH-Px活性明显高于模型组。结论：醒脑静注射液对大鼠颅脑损伤具有保护作用,其作用机制可能与减轻颅脑损伤后脑水肿及抑制氧自由基反应、保护神经细胞有关。     

The protective effect of ApolipoproteinA-I on myocardial ischemia-reperfusion injury in rats

It is well established that reperfusion of heart is the optimal method for salvaging ischemic myocardium, however, the success of this therapy could be limited by reperfusion injury, which is involved in inflammatory responses. High density lipoprotein (HDL) has an anti-inflammatory function and can protect the heart from ischemia-reperfusion (I/R) injury. In this study, we investigated the cardioprotective role of apolipoprotein A-I (ApoA-I), the major apolipoprotein of HDL, in I/R injury. Using rats subjected to myocardial I/R by ligation of left anterior descending coronary artery (LAD), we found that administration of ApoA-I (20 mg/kg, iv) before the onset of reperfusion of myocardial infarction can significantly reduce serum creatine kinase (CK) levels (62.1+/-13.8%, p<0.01) and heart TNF-alpha as well as IL-6 levels, compared with saline controls (40.4+/-14.7%, 44+/-9.8%, p<0.01 respectively). Moreover, ApoA-I treatment suppresses the expression of ICAM-1 on endothelium, thus diminishing neutrophil adherence, transendothelial migration, and the subsequent myocyte injury. We concluded that ApoA-I could effectively protect rat heart from I/R injury.     

Dynamin-related protein 1: A critical protein in the pathogenesis of neural system dysfunctions and neurodegenerative diseases

Mitochondria play a key role in the maintenance of neuronal function by continuously providing energy. Here, we will give a detailed review about the recent developments in regards to dynamin-related protein 1 (Drp1) induced unbalanced mitochondrial dynamics, excessive mitochondrial division, and neuronal injury in neural system dysfunctions and neurodegenerative diseases, including the Drp1 knockout induced mice embryonic death, the dysfunction of the Drp1-dependent mitochondrial division induced neuronal cell apoptosis and impaired neuronal axonal transportation, the abnormal interaction between Drp1 and amyloid β (Aβ) in Alzheimer's disease (AD), the mutant Huntingtin (Htt) in Huntington's disease (HD), and the Drp1-associated pathogenesis of other neurodegenerative diseases such as Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS). Drp1 is required for mitochondrial division determining the size, shape, distribution, and remodeling as well as maintaining of mitochondrial integrity in mammalian cells. In addition, increasing reports indicate that the Drp1 is involved in some cellular events of neuronal cells causing some neural system dysfunctions and neurodegenerative diseases, including impaired mitochondrial dynamics, apoptosis, and several posttranslational modification induced increased mitochondrial divisions. Recent studies also revealed that the Drp1 can interact with Aβ, phosphorylated τ, and mutant Htt affecting the mitochondrial shape, size, distribution, axonal transportation, and energy production in the AD and HD neuronal cells. These changes can affect the health of mitochondria and the function of synapses causing neuronal injury and eventually leading to the dysfunction of memory, cognitive impairment, resting tremor, posture instability, involuntary movements, and progressive muscle atrophy and paralysis in patients.