Neuroprotective effects and mechanisms of the YiQiWenYangSanHan formula on Parkinson's disease mice.

益气温阳三寒方对帕金森病小鼠的神经保护作用及其机制

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作者:Liu Jinling, Di Dong, Sun Suping, Sun Yan, Zhou Shihan, Liu Jing, Qin Zizhen, Yang Xinyu, Wang Xiao, Xu Zheng, Zhu Boran, Wu Haoxin
BACKGROUND: Parkinson's disease (PD) is a complex neurodegenerative disease, which is often treated with obvious side effects such as dopamine replacement therapy. Our team has validated the unique advantages of the traditional Chinese medicine formula, YiQiWenYangSanHan formula (YQWYSHF), through in vitro experiments, confirming its therapeutic potential for PD. Nevertheless, further research and validation are required to fully understand its protective effects and underlying mechanisms against PD. AIM OF THIS REVIEW: This study employed an in vivo model to investigate the effects of YQWYSHF on motor impairments, neuroinflammation, and mitochondrial dysfunction in C57BL/6 J mice caused by MPTP. MATERIALS AND METHODS: Sixty C57BL/6 J mice were randomly divided into 5 groups, all groups except the control group were intraperitoneally administered MPTP for 7 days (30 mg/kg). After 4 weeks of drug intragastric treatment, we assessed the dyskinesia of mice treated with different doses of YQWYSHF by behavioral examination. Additionally, immunofluorescence was used to examine the expression of ionized calcium binding adaptor protein 1 (IBA1) and glial fibrillary acidic protein-positive (GFAP) cells. Western blotting was used to assess the expression level of tyrosine hydroxylase (TH), pyrin domain-containing 3 protein (NLRP3), apoptosis-associated speck-like proteins (ASC), cysteine-containing aspartate protease-1 (Caspase-1), interleukin-1β (IL-1β), α-synuclein (α-syn), poly (ADP-ribose) polymerase 1 (PARP1), and poly ADP ribose (PAR). Furthermore, transmission electron microscopy revealed mitochondrial impairment in the neuronal cells of the substantia nigra (SN). RESULTS: YQWYSHF treatment alleviated dyskinesia in a mouse model of PD. Moreover, it increased the TH expression, and could reverse the increase of IBA1, GFAP, NLRP3, ASC, caspase-1,IL-1β, α-syn, PARP1 and PAR proteins induced by MPTP. CONCLUSIONS: YQWYSHF protects dopaminergic neurons in PD by attenuating neuroinflammation and mitochondrial dysfunction. This study provides new evidence for the clinical application of traditional Chinese medicine in the treatment of PD.

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