首页> 美国卫生研究院文献>Journal of Animal Science >334 Clostridium tyrobutyricum protect intestinal barrier function from LPS-induced apoptosis via p38/JNK signaling pathway in IPEC-J2
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334 Clostridium tyrobutyricum protect intestinal barrier function from LPS-induced apoptosis via p38/JNK signaling pathway in IPEC-J2

机译:334酪丁酸梭菌通过IPEC-J2中的p38 / JNK信号通路保护肠屏障功能免受LPS诱导的细胞凋亡

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摘要

Early weaning, a critical phase in swine production, can compromise intestinal barrier function through mucosal damage and alteration of tight junction integrity. Maintenance of intestinal barrier function plays a pivotal role in optimum gastrointestinal health. This study investigated the effects of Clostridium tyrobutyricum (C.t) on intestinal barrier dysfunction induced by lipopolysaccharide (LPS) and the underlying mechanisms. IPEC-J2 Cells were treated with PBS (the control), LPS (1 μg/mL for 12 h), C.t (10∧8 CFU/mL for 8 h), LPS + C.t (1 μg/mL LPS for 12 h followed by 10∧8 CFU/mL C.t for 8 h), or C.t + LPS (10∧8 CFU/mL C.t for 8 h followed by 1 μg/mL LPS for 12 h). The measurements of trans-epithelium electrical resistance values, tight junction proteins (TJs), apoptotic genes expressions, and MAPK expressions were determined after treatments. Statistical analysis was performed with one-way analysis of variance followed by Duncan multiple range test and differences were considered significant at P <0.05. The results showed that C.t efficiently maintained trans-epithelium electrical resistance values and intestinal permeability after LPS-induced intestinal barrier disruption (P <0.05). The expressions of TJs were enhanced when cells were treated with C.t (P <0.05). Fluorescence imaging and flow cytometry revealed that C.t inhibited cell apoptosis induced by LPS. C.t also increased the relative expression of the anti-apoptotic gene Bcl-2 and decreased that of the apoptotic genes Bax and caspase-3/-8 (P <0.05). The protective effect of C.t on damaged intestinal cell models was associated with suppression of p-p38 and p-JNK. Our findings suggest that C.t could protect against the LPS-induced increase in intestinal permeability and inhibit LPS-induced intestinal apoptosis via the p38/JNK signaling pathway in IPEC-J2 cells. These results suggest C.t is a potential probiotic additive for protecting the intestinal barrier and preventing diarrhea in early weaned piglets.
机译:早期断奶是猪生产中的关键阶段,可通过粘膜损伤和紧密连接完整性改变而损害肠道屏障功能。肠屏障功能的维持在最佳胃肠道健康中起着关键作用。这项研究调查了酪丁酸梭菌(C.t)对脂多糖(LPS)诱导的肠屏障功能障碍的影响及其潜在机制。 IPEC-J2细胞分别用PBS(对照),LPS(1μg/ mL进行12 h),Ct(10×8 CFU / mL进行8 h),LPS + Ct(1μg/ mL LPS进行12 h)处理(10×8 CFU / mL Ct持续8 h)或Ct + LPS(10×8 CFU / mL Ct持续8 h,然后1μg/ mL LPS持续12 h)。治疗后测定跨上皮电阻值,紧密连接蛋白(TJs),凋亡基因表达和MAPK表达的测量值。用单向方差分析进行统计学分析,然后进行邓肯多范围检验,差异被认为是显着的,P <0.05。结果表明,LPS诱导的肠屏障破坏后,C.t有效地维持了跨上皮的电阻值和肠通透性(P <0.05)。用C.t处理细胞后,TJs的表达增强(P <0.05)。荧光成像和流式细胞仪显示C.t抑制LPS诱导的细胞凋亡。 C.t还增加了抗凋亡基因Bcl-2的相对表达,并降低了凋亡基因Bax和caspase-3 / -8的相对表达(P <0.05)。 C.t对受损肠细胞模型的保护作用与抑制p-p38和p-JNK有关。我们的发现表明C.t可以通过IPEC-J2细胞中的p38 / JNK信号通路防止LPS诱导的肠通透性增加并抑制LPS诱导的肠凋亡。这些结果表明C.t是一种潜在的益生菌添加剂,可以保护早期断奶仔猪的肠道屏障并防止腹泻。

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