目的:基于IRE1α/JNK通路研究苁蓉舒痉颗粒对帕金森病(parkinson's disease,PD)模型大鼠的影响.方法:将45只雄性SD大鼠随机分成正常组、模型组和苁蓉舒痉颗粒组(5.21 g·kg-1),除正常组外,其余大鼠采用连续14 d颈背部皮下注射鱼藤酮葵花油乳化液(1.5 mg·kg-1)(按1.5∶1将鱼藤酮、葵花油配为鱼藤酮葵花油乳液)制备PD模型,连续给予相应的药物14 d.免疫组化法检测大鼠脑黑质酪氨酸羟化酶(tyrosine hydroxylase,TH)表达;Western Blot法检测大鼠脑额叶中IRE1α、JNK蛋白及其磷酸化的表达.结果:与模型组比较,苁蓉舒痉颗粒组大鼠脑黑质TH阳性细胞数明显增加(P＜0.05),脑额叶p-IRE1 α/IRE1α、p-JNK/JNK水平明显降低(P＜0.05).结论:苁蓉舒痉颗粒通过增加大鼠脑黑质TH阳性细胞数,降低脑额叶p-IRE1 α/IRE1α、p-JNK/JNK水平来保护神经细胞,可能与IRE1α/JNK通路有关.

目的:观察松果菊苷对帕金森病(PD)模型大鼠中脑超微结构的影响.方法:将健康SD大鼠随机分为对照组、模型组和松果菊苷组,每组10只.对照组用生理盐水灌胃,模型组和松果菊苷组大鼠造模后,分别用生理盐水和2 mg/mL的松果菊苷水溶液灌胃,每天1次,连续14 d.灌胃结束后,采集各组大鼠中脑,制作超薄切片,在7000倍和50000倍电镜下观察并比较各组大鼠中脑神经细胞超微结构的差异.结果:对照组中脑神经细胞结构清晰,核膜光滑、完整,核内染色质分布均匀;线粒体数量较多,形态规则,双层膜结构、线粒体嵴结构清晰.与对照组比较,模型组的神经细胞胞体缩小,核染色质边聚;线粒体数量减少,双层膜结构不清,线粒体嵴排列紊乱.松果菊苷组与模型组比较,神经细胞胞体大小有所恢复,核染色质边集现象有所缓解;线粒体数量增加,双层膜结构清晰,线粒体嵴排列相对规律,形态基本正常.结论:松果菊苷能改善PD模型大鼠中脑神经细胞凋亡的超微结构,这一结果可能与缓解神经细胞线粒体功能障碍有关.

This study investigated the effects of the Cong Rong Shu Jing (CRSJ) compound on endoplasmic reticulum stress in a rat model of Parkinson's disease (PD). A total of 40 rats were subcutaneously injected with rotenone-sunflower oil emulsion into the back of the neck to establish a rat model of PD. These PD rats were randomly divided into low-, medium-, and high-dose groups (intragastric administration of 0.5, 1, and 2 g/kg CRSJ, respectively) and a model group (intragastric administration of the solvent; 10 rats per group). Furthermore, 10 rats each were attributed to the control and vehicle groups (both received intragastric administration of the CRSJ solvent, and the vehicle group were injected additionally with sunflower oil alone). A traction test was conducted two times, after the PD model establishment and after 14 days of CRSJ gavage. The numbers of tyrosine hydroxylase- (TH-) positive cells and the dopamine levels in the substantia nigra were assessed using immunohistochemistry and high-performance liquid chromatography, respectively. Western blotting detected the expression levels of α-synuclein, endoplasmic reticulum stress pathways-related proteins, cerebral dopamine neurotrophic factor (CDNF), mesencephalic astrocyte-derived neurotrophic factor (MANF), and phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway-related proteins. Compared with the model group, the number of TH-positive cells in the substantia nigra was increased in the CRSJ groups. The expression levels of α-synuclein and the endoplasmic reticulum stress pathways-associated proteins glucose regulatory protein 78, inositol-requiring enzyme 1, apoptosis signal-regulating kinase 1, phosphorylated c-Jun N-terminal kinase, and caspase-12 were reduced. However, CRSJ administration elevated the expression levels of the neurotrophic factors CDNF and MANF, as well as those of p-PI3K and p-AKT. The CRSJ compound can relieve endoplasmic reticulum stress in PD rats and exerts protective effects in this animal model. These effects may be related to increased expression of neurotrophic factors and activation of the PI3K/AKT pathway.

The main pathological changes inherent in Parkinson's disease (PD) are degeneration and loss of dopamine neurons in the midbrain and formation of Lewy bodies. Many studies have shown that the pathogenesis of PD is closely related to endoplasmic reticulum (ER) oxidative stress. This study combined various traditional Chinese medicines to prepare Congrong Shujing granules (CSGs). The optimal dose combination of the ingredients was identified by experimental intervention in SH-SY5Y cells in vitro. A PD rat model was established by intraperitoneal injection of rotenone sunflower oil emulsion. The suspension tests were performed on the 14th day after modeling and also on the 14th day after CSG intervention (5.88 g/kg, 11.76 g/kg, and 23.52 g/kg). We evaluated the changes in motor function and the expression of neuronal cell functional marker proteins, ER stress (ERS) marker proteins, and apoptosis-related pathway proteins of neuronal cells. Changes in cellular ultrastructure were observed by electron microscopy. Our results showed that CSG treatment lengthened the duration of PD rats' gripping to the wire. 78 kDa glucose-regulated protein (GRP78) expression in the substantia nigra was significantly upregulated in the middle- and high-dose CSG groups after 14 days of treatment compared with the model group. The expression of the key dopaminergic neuron functional enzyme tyrosine hydroxylase (TH) and cerebral dopamine neurotrophic factor (CDNF) was elevated. The expression of c-Jun N-terminal kinase (JNK) and phosphorylated c-Jun decreased, and cell apoptosis was significantly reduced. Compared with the model group, the treatment groups had fewer ER fragmentation and degranulation (ribosome shedding) and abundant ER and mitochondria suggesting that CSG reduced ER stress and neuronal apoptosis in the midbrain of a PD rat model by inducing the expression of molecular chaperone GRP78.

目的 观察松果菊苷对帕金森病模型大鼠纹状体葡萄糖调节蛋白78(GRP78)及中脑星形胶质细胞源性神经营养因子(MANF)蛋白含量的影响.方法 32只雄性SD大鼠随机分为正常组、溶剂组及造模组.连续颈背部皮下注射鱼藤酮葵花油乳化液14d建立帕金森病大鼠模型,将造模成功的大鼠随机分为模型组与治疗组,每组8只.治疗组予以松果菊苷20mg/(kg·d)灌胃.其余各组予以等量生理盐水灌胃,连续给药14d.各组大鼠于松果菊苷治疗前1d及治疗14d后行悬挂试验;药物干预结束后,麻醉下处死大鼠取纹状体,蛋白质印迹法(Western Blot)检测GRP78及MANF蛋白的表达.结果 治疗前1d,模型组及治疗组大鼠悬挂时间较正常组缩短(P<0.01);治疗14d后,治疗组大鼠悬挂时间较模型组延长(P<0.05).与正常组比较,模型组GRP78蛋白表达增高,MANF蛋白表达降低(P<0.05);与模型组比较,治疗组GRP78蛋白表达降低,MANF蛋白表达升高(P<0.05).结论 松果菊苷可能通过调节内质网应激相关蛋白GRP78表达及增加MANF的表达改善帕金森病的行为障碍.

目的 研究苁蓉精对帕金森病模型大鼠延髓中PI3 K/AKT通路的影响,探讨苁蓉精改善帕金森病相关症状可能的机制.方法 将造模成功的24只SD大鼠随机分为模型组、苁蓉精40,80,160 mg·Kg-1·d-1三个剂量组,并设立正常组与假手术组,每组6只;分别给予苁蓉精或生理盐水,连续灌胃14天.Western Blotting检测大鼠延髓AKT、PI3K及P-AKT、P-PI3K蛋白的表达.结果 与正常组比较,PD模型组大鼠延髓中P-AKT、p-PI3K蛋白的表达量降低(P＜0.05);与模型组对比,给药组PD模型大鼠中80、160 mg·Kg-1 · d-1剂量组的p-AKT蛋白的表达量明显增高(P＜0.05),而40、80、160 mg·Kg-1·d-1三个剂量组中P-PI3K蛋白的表达量都明显增高,且具有量效依赖关系(P＜0.05).结论:苁蓉精可提高延髓中P-AKT、P-PI3K蛋白的表达量对神经元起到保护作用.

大数据是信息化、网络化、智能化的核心.中医健康管理从数据采集、数据传递到数据处理,都与大数据密不可分.文章分析了中医健康管理产生大数据的背景情况,阐述了大数据对中医健康管理将发挥的促进作用,并进一步探讨了中医健康管理大数据应用面临的问题.文章最后指出多学科交叉融合是中医健康管理与大数据健康发展的必然趋势.

目的 研究苁蓉舒痉方对鱼藤酮所致帕金森病模型大鼠纹状体Akt、P-Akt、mTOR表达的影响.方法 用鱼藤酮葵花油乳液制备帕金森病大鼠模型,将造模成功的大鼠随机分为模型组、低剂量组、中剂量组、高剂量组,应用Westem blot方法检测大鼠纹状体中Akt、P-Akt和mTOR的含量变化. 结果 Western blot检测结果显示,模型组大鼠纹状体的Akt、P-Akt蛋白表达减少(P＜0.05);与模型组比较,中剂量组P-Akt蛋白表达增加(P＜0.05),高剂量组Akt、mTOR蛋白表达增加(P＜0.05). 结论 苁蓉舒痉方可提高帕金森病模型大鼠纹状体Akt、P-Akt和mTOR的表达,激活Akt/mTOR通路,可能是减轻大脑纹状体多巴胺神经元损伤的作用机制之一.