Effect of Puerarin, Baicalin and Berberine Hydrochloride on the Regulation of IPEC-J2 Cells Infected with Enterotoxigenic Escherichia coli

Effect of Puerarin, Baicalin and Berberine Hydrochloride on the Regulation of IPEC-J2 Cells Infected with Enterotoxigenic Escherichia coli
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葛根素、黄芩苷和盐酸小檗碱对产肠毒素大肠杆菌感染IPEC-J2细胞的调节作用

DOI:
10.1155/2019/7438593
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发表时间:
2019-01-01
影响因子:
--
通讯作者:
Xu, Jianqin
Xu, Jianqin
中科院分区:
医学4区
文献类型:
--
作者:
Liu, Xiaoxi;Liu, Fenghua;Xu, Jianqin

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葛根素、黄芩苷和盐酸小檗碱的主要组件是对战Qinlian煎煮,已用于治疗腹泻在中国数百年来,然而这些组件的生物功能和分子机制尚不清楚。探讨葛根素、黄芩苷和盐酸小檗碱对感染肠产毒素大肠杆菌(ETEC)的猪肠上皮细胞(IPEC-J2细胞)的调控作用。用葛根素(200 μg/mL)、黄芩苷(1 μg/mL)、盐酸小檗碱(100 μg/mL)在37℃条件下预处理IPEC-J2细胞3 h,再与F4ac ETEC菌株200在37℃条件下共孵育3 h。ETEC感染后IPEC-J2细胞结构破坏,mucin 4和mucin 13 mRNA表达上调(P < 0.01),凋亡率升高(P < 0.05);通过激活核因子-κB (NF-κB)信号通路,促进IPEC-J2细胞的炎症反应(IL-6和CXCL-2 mRNA表达)。葛根素、黄芩苷和盐酸小檗碱预处理改善了IPEC-J2细胞的结构和形态,并通过下调特异性粘附分子抑制ETEC粘附。黄芩苷预处理可降低炎症反应;黄芩苷和盐酸小檗碱预处理可降低NF-κB信号通路介导的炎症反应。葛根素、黄芩苷和盐酸小檗碱预处理通过抑制细菌粘附和炎症反应来保护IPEC-J2细胞免受ETEC感染。
Puerarin, baicalin and berberine hydrochloride are the main components of Gegen Qinlian Decoction, which has been used to treat diarrhoea in China for hundreds of years, yet the biological function and molecular mechanism of these components are not clear. To investigate the effects of puerarin, baicalin, and berberine hydrochloride on the regulation of porcine intestinal epithelial cells (IPEC-J2 cells) infected with enterotoxigenic Escherichia coli (ETEC). IPEC-J2 cells were pretreated with puerarin (200 μg/mL), baicalin (1 μg/mL), and berberine hydrochloride (100 μg/mL) at 37°C for 3 h and then coincubated with the F4ac ETEC bacterial strain 200 at 37°C for 3 h. ETEC infection damaged the structure of IPEC-J2 cells, upregulated mucin 4 (P < 0.01) and mucin 13 mRNA (P < 0.05) expression, increased the apoptosis rate (P < 0.05), and promoted inflammatory responses (IL-6 and CXCL-2 mRNA expression) in IPEC-J2 cells by activating the nuclear factor-κB (NF-κB) signaling pathway. Pretreatment with puerarin, baicalin, and berberine hydrochloride improved the structure and morphology of IPEC-J2 cells and inhibited ETEC adhesion by downregulating specific adhesion molecules. Pretreatment with baicalin decreased the inflammatory response; pretreatment with baicalin and berberine hydrochloride decreased the inflammatory response mediated by the NF-κB signaling pathway. Pretreatment with puerarin, baicalin, and berberine hydrochloride protected IPEC-J2 cells from ETEC infection by inhibiting bacterial adhesion and inflammatory responses.