Sesamin Protects against and Ameliorates Rat Intestinal Ischemia/Reperfusion Injury with Involvement of Activating Nrf2/HO‐1/NQO1 Signaling Pathway | Zendy

Yilin Wang | Zendy; Jin Wen | Zendy; Marwan Almoiliqy | Zendy; Yaojia Wang | Zendy; Zhihao Liu | Zendy; Xiaobo Yang | Zendy; XiaoLong Lu | Zendy; Qiang Meng | Zendy; Jinyong Peng | Zendy; Yuan Lin | Zendy; Pengyuan Sun | Zendy

Open Access

Sesamin Protects against and Ameliorates Rat Intestinal Ischemia/Reperfusion Injury with Involvement of Activating Nrf2/HO‐1/NQO1 Signaling Pathway

Author(s) -

Yilin Wang,

Jin Wen,

Marwan Almoiliqy,

Yaojia Wang,

Zhihao Liu,

Xiaobo Yang,

XiaoLong Lu,

Qiang Meng,

Jinyong Peng,

Yuan Lin,

Pengyuan Sun

Publication year - 2021

Publication title -

oxidative medicine and cellular longevity

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.494

H-Index - 93

eISSN - 1942-0900

pISSN - 1942-0994

DOI - 10.1155/2021/5147069

Subject(s) - sesamin , reperfusion injury , signal transduction , chemistry , ischemia , pharmacology , microbiology and biotechnology , medicine , biochemistry , biology , food science

Intestinal ischemia-reperfusion (I/R) may induce cell/tissue injuries, leading to multiple organ failure. Based on our preexperiments, we proposed that sesamin could protect against and ameliorate intestinal I/R injuries and related disorders with involvement of activating Nrf2 signaling pathway. This proposal was evaluated using SD intestinal I/R injury rats in vivo and hypoxia/reoxygenation- (H/R-) injured rat small intestinal crypt epithelial cell line (IEC-6 cells) in vitro . Sesamin significantly alleviated I/R-induced intestinal histopathological injuries and significantly reduced serum biochemical indicators ALT and AST, alleviating I/R-induced intestinal injury in rats. Sesamin also significantly reversed I/R-increased TNF- α , IL-6, IL-1 β , and MPO activity in serum and MDA in tissues and I/R-decreased GSH in tissues and SOD in both tissues and IEC-6 cells, indicating its anti-inflammatory and antioxidative stress effects. Further, sesamin significantly decreased TUNEL-positive cells, downregulated the increased Bax and caspase-3 protein expression, upregulated the decreased protein expression of Bcl-2 in I/R-injured intestinal tissues, and significantly reversed H/R-reduced IEC-6 cell viability as well as reduced the number of apoptotic cells among H/R-injured IEC-6 cell, showing antiapoptotic effects. Activation of Nrf2 is known to ameliorate tissue/cell injuries. Consistent with sesamin-induced ameliorations of both intestinal I/R injuries and H/R injuries, transfection of Nrf2 cDNA significantly upregulated the expression of Nrf2, HO-1, and NQO1, respectively. On the contrary, either Nrf2 inhibitor (ML385) or Nrf2 siRNA transfection significantly decreased the expression of these proteins. Our results suggest that activation of the Nrf2/HO-1/NQO1 signaling pathway is involved in sesamin-induced anti-inflammatory, antioxidative, and antiapoptotic effects in protection against and amelioration of intestinal I/R injuries.

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