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Qian J, Wang X, Weng W, et al. Salidroside alleviates taurolithocholic acid 3-sulfate-induced AR42J cell injury. Biomed Pharmacother. 2021;142:112062doi: 10.1016/j.biopha.2021.112062.
Qian, J., Wang, X., Weng, W., Zhou, G., Zhu, S., & Liu, C. (2021). Salidroside alleviates taurolithocholic acid 3-sulfate-induced AR42J cell injury. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 142112062. https://doi.org/10.1016/j.biopha.2021.112062
Qian, Jing, et al. "Salidroside alleviates taurolithocholic acid 3-sulfate-induced AR42J cell injury." Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie vol. 142 (2021): 112062. doi: https://doi.org/10.1016/j.biopha.2021.112062
Qian J, Wang X, Weng W, Zhou G, Zhu S, Liu C. Salidroside alleviates taurolithocholic acid 3-sulfate-induced AR42J cell injury. Biomed Pharmacother. 2021 Oct;142:112062. doi: 10.1016/j.biopha.2021.112062. Epub 2021 Aug 21. PMID: 34435589.
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Biomed Pharmacother. 2021 Oct;142:112062. doi: 10.1016/j.biopha.2021.112062. Epub 2021 Aug 21.

Salidroside alleviates taurolithocholic acid 3-sulfate-induced AR42J cell injury.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

Jing Qian, Xiaohong Wang, Wenjun Weng, Guoxiong Zhou, Shunxing Zhu, Chun Liu

Affiliations

  1. Department of General Surgery, Yizheng Hospital of Nanjing Drum Tower Hospital Group, Yizheng 211900, Jiangsu, China. Electronic address: [email protected].
  2. Department of Gastroenterology, Yizheng Hospital of Nanjing Drum Tower Hospital Group, Yizheng 211900, Jiangsu, China. Electronic address: [email protected].
  3. Department of Cardiothoracic Surgery, Yizheng Hospital of Nanjing Drum Tower Hospital Group, Yizheng 211900, Jiangsu, China. Electronic address: [email protected].
  4. Department of Gastroenterology, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu, China. Electronic address: [email protected].
  5. Laboratory Animal Center of Nantong University, Nantong 226001, Jiangsu, China. Electronic address: [email protected].
  6. Laboratory Animal Center of Nantong University, Nantong 226001, Jiangsu, China. Electronic address: [email protected].

PMID: 34435589 DOI: 10.1016/j.biopha.2021.112062

Abstract

OBJECTIVES: To investigate the protective effects of Salidroside (Sal) on AP cell model induced by taurolithocholic acid 3-sulfate (TLC-S) as well as its underlying mechanism.

METHODS: AR42J cells were divided into normal group (N group), AP cell model group (Mod group), Sal treated alone group (S+N group) and Sal treated AP cell model group (S+Mod group). The cell viability was examined by CCK-8 assay. Secretion of lipase and trypsin by AR42J cells, quantified using commercial assay kits, was used as the markers of TLC-S-induced pancreatitis. The levels of TNF-α, IL-1β, IL-8, IL-6 and IL-10 in the cell supernatant were measured by ELISA. The effect of Sal on molecules in the NF-κB signaling pathway and autophagy was investigated by qRT-PCR and western blot.

RESULTS: The decreased cell viability in Mod group was increased by Sal (P < 0.01). The upheaved activities of lipase and trypsin in AP cell model were declined by Sal (P < 0.01). The levels of TNF-α, IL-1β, IL-8 and IL-6 in the cell supernatant, Beclin-1 and LC3-Ⅱ mRNA and protein, p-p65/p65 protein, which were increased in AP cell model, were decreased by Sal; and IL-10 in the cell supernatant, LAMP2 mRNA and protein, p-IκBα/IκBα protein which was declined in AP cell model, was increased by Sal (P < 0.05 or 0.01). There were no significant differences in all indexes between the N and S+N groups (P > 0.05).

CONCLUSIONS: Sal alleviated AR42J cells injury induced by TLC-S, inhibited the inflammatory responses and modulated the autophagy, mainly through inhibiting the NF-κB signaling pathway.

Copyright © 2021 The Authors. Published by Elsevier Masson SAS.. All rights reserved.

Keywords: AR42J cell; Autophagy; Inflammatory response; Nuclear factor kappa B; Salidroside; Taurolithocholic acid 3-sulfate

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