In this review,we summarize the involvement of vitamin C in mental disorders by presenting available evidence on its pharmacological effects in animal models as well as in clinical studies.Vitamin C,especially its reduced form,has gained interest for its multiple functions in various tissues and organs,including central nervous system（CNS）.Vitamin C protects the neuron against oxidative stress,alleviates inflammation,regulates the neurotransmission,affects neuronal development and controls epigenetic function.All of these processes are closely associated with psychopathology.In the past few decades,scientists have revealed that the deficiency of vitamin C may lead to motor deficit,cognitive impairment and aberrant behaviors,whereas supplement of vitamin C has a potential preventive and therapeutic effect on mental illness,such as major depressive disorder（MDD）,schizophrenia,anxiety and Alzheimer＇s disease（AD）.Although several studies support a possible role of vitamin C against mental disorders,more researches are essential to accelerate the knowledge and investigate the mechanism in this field.
Mitochondrial superoxide overproduction is believed to be responsible for the neurotoxicity associated with neurodegeneration.Mitochondria-targeted antioxidants,such as MitoQ,have emerged as potentially effective antioxidant therapies.Methionine sulfoxide reductase A(MsrA)is a key mitochondrial-localized endogenous antioxidative enzyme and it can scavenge oxidizing species by catalyzing the methionine(Met)-centered redox cycle(MCRC).In this study,we observed that the natural L-Met acted as a good scavenger for antimycin A-induced mitochondrial superoxide overproduction in PC12 cells.This antioxidation was largely dependent on the Met oxidase activity of MsrA.S-methyl-L-cysteine(SMLC),a natural analogue of Met that is abundantly found in garlic and cabbage,could activate the Met oxidase activity of MsrA to scavenge free radicals.Furthermore,SMLC protected against antimycin A-induced mitochondrial membrane depolarization and alleviated 1-methyl-4-phenylpyridinium(MPP+)-induced neurotoxicity.Thus,our data highlighted the possibility for SMLC supplement in the detoxication of mitochondrial damage by activating the Met oxidase activity of MsrA.
目的探讨精神分裂症社区康复技术对患者自知力及社会功能康复的作用。方法将280例社区精神分裂症患者随机分为干预组(140例)和对照组(140例),干预组患者分组进行康复干预4周,对照组患者进行社区常规康复干预和健康教育。两组共269例患者完成12个月的随访。入组后分别于基线、随访6个月末、随访12个月末评定1次自知力与治疗态度问卷(insight and treatment attitude questionnaire,ITAQ)、个人与社会功能量表(personal and social performance scale,PSP)。结果 1重复测量方差分析结果显示,随访6个月和12个月,干预组患者ITAQ总分均高于对照组(P<0.001);2干预组患者末次随访PSP评分较基线增加分值高于对照组增加分值(P<0.05);3干预组患者复发率和住院率均低于对照组(P<0.001,P<0.05)。结论精神分裂症社区康复技术能够显著提高患者的自知力,改善其社会功能,有效预防复发并降低住院风险,具有社区推广意义。
目的探讨抑郁症康复技能训练对抑郁症患者症状缓解及生活质量的效果。方法把212例符合入组标准的抑郁症患者,采用分层随机分组的方法分为技能训练组(102例)和健康教育组(110例)。技能训练组接受抑郁症康复技能训练程式干预,健康教育组接受抑郁症相关知识讲座,对两组患者均随访观察1年。每3个月对两组患者进行随访评估,评估工具包括:一般情况调查表、17项汉密尔顿抑郁量表(Hamilton Depression Rating Scale for Depression-17 item,HAMD-17)、世界卫生组织生存质量测定量表简表(World Health Organization's Quality of Life Instruments-Abbreviated Version,WHOQOL-BREF)。采用SPSS 17.0统计软件进行数据分析。结果 (1)HAMD-17总分组间和组内差异均有统计学意义,技能训练组随访时点3、6、9、12个月均显著低于健康教育组(均P <0.05)。(2)WHOQOL-BREF自评总分及生存质量自评、健康状况满意度自评组间和组内差异均有统计学意义,技能训练组随访时点6、9、12个月各因子分均高于健康教育组(均P <0.05)。结论抑郁症康复技能训练程式能有效缓解抑郁症患者症状,促进患者生活质量提高。
