Protective Effect of Pretreatment of Astragalus membranaceus Injection at Five Zang-Organ Shu Acupoints in D-gal–Induced Aging Rats

氧化应激 丙二醛 腹腔注射 超氧化物歧化酶 内科学 内分泌学 医学 抗氧化剂 病态的 药理学 衰老 海马体 下调和上调 歧化酶 免疫组织化学 氧化损伤 化学
作者
Shan Zhong,Xilin Wang,Yuan Guo,Jingren Chen,Qing Lin,Shumin Wen,Yuhong Chen,Songzhe He,Shan Zhong,Xilin Wang,Yuan Guo,Jingren Chen,Qing Lin,Shumin Wen,Yuhong Chen,Songzhe He
出处
期刊:Acupuncture & electro-therapeutics research [Cognizant]
卷期号:49 (4): 242-256
标识
DOI:10.1177/03601293251356851
摘要

Background Aging is a progressive process associated with the decline of both cell structure and function, involving oxidative stress as well as mitochondrial dysfunction. However, strategies to delay the aging process have become a research hotspot that an increasing number of researchers are focusing on. This study aimed to explore the protective effect of pretreatment of Astragalus membranaceus (AM) injection at five Zang-organ Shu acupoints in D-galactose (D-gal)–induced aging rats. Methods The rats received acupoint injections of the five Zang-organ Shu acupoints [Feishu (BL 13), Xinshu (BL 15), Ganshu (BL 18), Pishu (BL 20), and Shenshu (BL 23)] with AM injection prior to intraperitoneal injection of D-gal. Organ indexes, biochemical serum parameters, histopathological morphology, and aging-related protein levels of the brain and kidney tissues were used to evaluate the oxidative alterations induced by D-gal and the protective role of AM injection. Results AM injection improved organ indexes, biochemical serum parameters, and the pathological damage of the brain and kidney tissues. Primary mechanism analysis showed that AM injection decreased the expression of aging markers (p53 and p16) in the hippocampus of aging rats. Furthermore, AM injection significantly decreased malondialdehyde (MDA) levels and increased superoxide dismutase (SOD) activity, enhancing the antioxidant status. Conclusion Pretreatment of AM injection at five Zang-organ Shu acupoints ameliorates oxidative stress induced by D-gal in the rats through downregulation of aging markers (p53 and p16), a decrease in SOD activity, and an increase in MDA content.

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