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该粉末通过连接蛋白 43(Cx43)/糖皮质激素受体/脑源性神经营养因子信号通路缓解慢性不可预测轻度应激诱导的抑郁模型大鼠海马区的海马神经元损伤。

powder alleviates the hippocampal neuron damage in chronic unpredictable mild stress-induced depression model rats in hippocampus via connexin 43Cx43/glucocorticoid receptor/brain-derived neurotrophic factor signaling pathway.

机构信息

South China Research Center for Acupuncture and Moxibustion, Medical College of Acu-Moxi and Rehabilitation, Guangzhou University of Chinese Medicine, Guangzhou City, China.

Centre for Integrative Medicine, School of Basic Medical Science, Guangzhou University of Chinese Medicine, Guangzhou City, China.

出版信息

Bioengineered. 2022 Jan;13(1):383-394. doi: 10.1080/21655979.2021.2005744.

Abstract

Powder (XYP) has been widely applied in China to treat stress-related illnesses, such as migraine, depression, Parkinson's disease, insomnia, and hypertension. Herein, this study aims to explore the effect of XYP on chronic unpredictable mild stress (CUMS)-induced depression and its underlying mechanisms. CUMS-induced depression rat models were established, they were subsequently randomly divided and treated with various conditions. Results of this study indicated that supplementation of XYP observably abolished CUMS-induced hippocampal damage and serum corticosterone (CORT) elevation. In mechanism, we discovered that CUMS induction could cause a prominent downregulation in glucocorticoid receptor (GR), phosphorylated-GR (p-GR), connexin 43 (Cx43), and brain-derived neurotrophic factor (BDNF), a remarkable upregulation in c-Src. While the introduction of XYP could reverse the changes in all of these indicators mediated by CUMS. Furthermore, we proved that Cx43 could interact with GR, and the protective effect of XYP on hippocampal neurons is realized by up-regulating GR. Summarized, this study indicated that XYP could ameliorate hippocampal neuron damage in CUMS-induced depression model rats through acting on Cx43/GR/BDNF axis.

摘要

(XYP)粉末已在中国广泛用于治疗与压力相关的疾病,如偏头痛、抑郁症、帕金森病、失眠和高血压。在此,本研究旨在探讨 XYP 对慢性不可预测轻度应激(CUMS)诱导的抑郁症的影响及其潜在机制。建立了 CUMS 诱导的抑郁症大鼠模型,随后将其随机分组并给予不同的处理。研究结果表明,XYP 的补充显著消除了 CUMS 诱导的海马损伤和血清皮质酮(CORT)升高。在机制上,我们发现 CUMS 诱导会导致糖皮质激素受体(GR)、磷酸化-GR(p-GR)、连接蛋白 43(Cx43)和脑源性神经营养因子(BDNF)明显下调,原癌基因 c-Src 明显上调。而 XYP 的引入可以逆转 CUMS 介导的所有这些指标的变化。此外,我们证明 Cx43 可以与 GR 相互作用,XYP 通过上调 GR 对海马神经元发挥保护作用。综上所述,本研究表明,XYP 可以通过作用于 Cx43/GR/BDNF 轴来改善 CUMS 诱导的抑郁症模型大鼠的海马神经元损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cbed/8805874/c81fb0c8a15e/KBIE_A_2005744_F0001_OC.jpg

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