Based on molecular docking to evaluate the protective effect of saponins from ginseng berry on D-gal-induced brain injury via multiple molecular mechanisms in mice. (October 2022)

• Record Type: Journal Article
• Authors: Liu, Yong-bo; Sun, Da-zhong; Chen, Ke-cheng; Zhang, Jun-jie; Hou, Yun-yi; Gao, Xu-fei; Cai, En-bo; Zhu, Hong-Yan; Zheng, Yi-nan; Chen, Ri-xin; Liu, Shuang; Li, Wei
• Is Part Of: Journal of functional foods. Volume 97(2022)
• Publication Date: 2022-10
• Subjects: Ginsenosides -- Ginseng berry -- D-galactose -- Oxidative stress -- Cell aging; GBS ginseng berry saponins -- D-gal D-galactose -- AChE acetylcholinesterase -- ChAT choline acetyltransferase -- CAT catalase -- MDA malondialdehyde -- SIRT1 silencing information regulator 1 -- Akt protein kinase B -- H&E Hematoxylin and eosin -- MWM Morris water maze; Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2022.105224
• Languages: English
• ISSNs: 1756-4646

Abstract

Graphical abstract: Highlights: To explore the effect of ginseng berries saponins on D-gal-induced brain injury. The content of various saponins in ginseng berries was quantitatively analyzed. Ginseng berry saponins can improve oxidative stress, apoptosis and cell aging. Ginseng berry saponins may activate the SIRT1/Akt signaling pathway. Abstract: The present study investigated the protective effects of crude saponins (ginsenosides) in berries in an brain injury model by intraperitoneal injection of D-gal (D-galactose). Our study showed that ginseng berry saponin (GBS) treatment significantly improved memory impairment in mice. Meanwhile, long-term exposure to D-gal reduces the expression of cholinergic modulators such as choline acetyltransferase (ChAT) and acetylcholinesterase (AChE), which can be significantly improved after administration. Furthermore, we found that GBS improved redox levels in the brain. In addition, TUNEL staining results showed that GBS inhibited D-Gal-induced apoptosis. Finally, we found that GBS treatment delayed cell aging by modulating the expression levels of cyclin D1 and senescence proteins p16 and p21, and further attenuated oxidative stress by activating SIRT1/Akt pathway. These results suggest that GBS can effectively treat D-Gal-induced brain damage and may be a potential therapeutic agent for slowing down the aging process.