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Saponins from the roots of Platycodon grandiflorum, an edible medicinal plant, have shown a wide range of beneficial effects on various biological processes. In this study, an animal model was established by a single intraperitoneal injection of cisplatin (20 mg/kg) for evaluating the protective effects of saponins from the roots of P. grandiflorum (PGS, 15 mg/kg and 30 mg/kg) in mice. The results indicated that PGS treatment for 10 days restored the destroyed intestinal mucosal oxidative system, and the loosened junctions of small intestinal villi was significantly improved. In addition, a significant mitigation of apoptotic effects deteriorated by cisplatin exposure in small intestinal villi was observed by immunohischemical staining. Also, western blot showed that PGS could effectively prevent endoplasmic reticulum (ER) stress-induced apoptosis caused by cisplatin in mice by restoring the activity of PERK (an ER kinase)-eIF2 α -ATF4 signal transduction pathway. Furthermore, molecular docking results of main saponins in PGS suggested a better binding ability with target proteins. In summary, the present work revealed the underlying protective mechanisms of PGS on intestinal injury induced by cisplatin in mice. [ABSTRACT FROM AUTHOR]

[Display omitted] • This paper is the first to investigate the protective effect of arabinogalactan on cisplatin-induced renal injury through network pharmacology and in vivo experiments. • This study illustrates that cisplatin stimulates the release of excessive ROS in the body to induce oxidative stress, which in turn triggers apoptosis in renal cells. • This study is the first to investigate the protective effect of arabinogalactan on the kidney in terms of the mechanism of oxidative stress and apoptosis. Cisplatin is the most widely used anticancer chemotherapy drug at present. However, its severe nephrotoxic side effects limit the clinical application. This study aimed to investigate the potential protective mechanism of arabinogalactan (AG) on acute kidney injury (AKI) induced by cisplatin in mice. Firstly, 105 potential targets of AG were predicted by using the SwissTargetPrediction database, 25,183 kidney disease targets were obtained by searching 5 disease databases, and 100 cross-target targets were obtained by drawing a Venn diagram. We constructed the "AG-Key target" interaction network and PPI protein interaction network of cross-targets and screened out 21 core targets. Through the GO and KEGG enrichment analysis of the core targets, we can found that the core targets involved a total of 1254 biological functions and 56 signaling pathways, including the apoptosis signaling pathway. By establishing an animal model in vivo , we found that pretreatment with AG at doses of 200 and 400 mg/kg could decrease the kidney index, such as serum creatinine (CRE), and blood urea nitrogen (BUN) levels induced by cisplatin, and reduce the kidney histopathology injury. Importantly, AG could inhibit the formation of metaldehyde (MDA) and 4-hydroxynonenal (4-HNE) in the kidney tissues and reduce the oxidative stress injury induced by cisplatin. Meanwhile, AG also restored the expression of anti-apoptotic proteins Bcl-2 and Bcl-xL and decreased the expression of pro-apoptotic proteins Bax and Bad in cisplatin-induced renal tissues. Finally, AG could further reduce cisplatin-induced kidney cell apoptosis. [ABSTRACT FROM AUTHOR]