Berberine induces ZIP14 expression and modulates zinc redistribution to protect intestinal mucosal barrier during polymicrobial sepsis

Publication date: 15 September 2019Source: Life Sciences, Volume 233Author(s): Yan He, Xiaoming Yuan, Hao Zuo, Xiangwei Li, Ying Sun, Aiwen FengAbstractAimsThe present study investigated if berberine might induce Zrt-Irt-like protein 14 (ZIP14) and affect zinc redistribution to protect intestinal barrier in sepsis.Main methodsRodent model of sepsis was induced by cecal ligation and puncture (CLP). Plasma endotoxin was assayed by LAL test and plasma zinc was measured by flame atomic spectrophotometer. Gut mucosal permeability was determined by plasma FITC-dextran. Zinc content and ZIP14 mRNA in gut mucosa were assayed by spectrophotometer and qRT-PCR, respectively. Tight junction integrity of Caco-2 was evaluated by transepithelial electrical resistance (TEER). Tight junction (TJ) protein expression was detected by Western blotting.Key findingsBerberine and zinc gluconate pretreatment to CLP rats improved survival rate, reduced plasma endotoxin level, alleviated hypozincemia, increased zinc accumulation and ZIP14 mRNA expression in the intestinal mucosa. Berberine and zinc gluconate pretreatment decreased CLP-elicited intestinal hyperpermeability to FITC-dextran. These effects of berberine in vivo were abolished by AG1024. In vitro, lipopolysaccharide (LPS) repressed zinc transfer into Caco-2 cells exposed to zinc gluconate. Berberine and IGF-I treatment increased ZIP14 protein expression and promoted zinc transfer into Caco-2 cells exposed to zinc gluconate plus LPS. Berberin...

Source: Life Sciences - July 31, 2019 Category: Biology Source Type: research