LBP Attenuate Heat Stroke-induced Colonic Injury in Rats by Inhibiting Ferroptosis through Nrf2/GPX4 Pathway
Objective This study aims to investigate the protective effects of Lycium barbarum polysaccharides(LBP)on colonic tissues of rats with heat stroke and the impact on the expression levels of Nrf2,GPX4,xCT,and other related factors.Methods Forty male of SPF-grade rats at the age of 6 weeks were randomly divided into the following groups:blank control(Con)group,heat stroke(HS)group,and low,medium,and high-dose[50,150,450 mg·(kg·d)-1]LBP groups.The Con and HS groups were administered with pure water,while the remaining groups were administered with LBP aqueous solution for a period of 4 weeks.After the gavage period,heat stroke was induced in rats,and tissue samples were collected.HE and PAS staining were used to evaluate the pathological changes in colonic tissues.TBA method was employed to detect MDA levels CAT levels and SOD levels in serum and tissues.Immunofluorescence was used to validate the expression changes of Occludin and ZO-1 proteins in transverse colonic tissues after LBP intervention.Western blot was utilized to verify the expression changes of GPX4,xCT,and Nrf2 proteins.Results Compared to the Con group,the colonic mucos-al structure in the HS group was observed to he damaged.With the increase in LBP dosage,the severity of colonic mucosal damage caused by heat stress significantly decreased(P＜0.05),and antioxidant levels in colonic tissues and serum gradually recovered to the levels of the Con group(P＜0.05).Compared to the Con group,the expression of Occludin,ZO-1,GPX4,and xCT proteins in colonic tissues decreased in the HS group(P all＜0.05)and significantly increased in the high-dose LBP group(P＜0.05).Meanwhile,the level of Nrf2 pro-tein significantly increased in the HS group after stress(P＜0.05)and continued to rise to a higher level in the high-dose LBP group(P＜0.05).Conclusion LBP activates Nrf2,inhibits ferroptosis by upregulating antioxi-dant factors GPX4 and xCT,and thus antagonizes the colon damage caused by the decreased level of tight junc-tion protein in the rat model of thermal radiation disease.
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