Probiotic Lactobacillus casei Zhang reduces pro-inflammatory cytokine production and hepatic inflammation in a rat model of acute liver failure
Probiotic Lactobacillus casei Zhang reduces pro-inflammatory cytokine production and hepatic inflammation in a rat model of acute liver failure
复制标题
益生菌干酪乳杆菌可减少急性肝衰竭大鼠模型中促炎细胞因子的产生和肝脏炎症。
DOI：
10.1007/s00394-015-0904-3
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发表时间：
2016-03-01
影响因子：
5
通讯作者：
Zhang, Heping
中科院分区：
文献类型：
--
作者：
Wang, Yuzhen;Xie, Jiming;Zhang, Heping
目的：本研究旨在探讨益生菌干酪乳杆菌（L. casei Zhu）对脂多糖（LPS）和D-半乳糖胺（GalN）诱导的急性肝衰竭大鼠模型中促炎细胞因子产生和肝脏炎症反应的影响和机制。方法：雄性Wistar大鼠经口给予或不给予 L. casei Zhang 在用 LPS 和 GalN 攻击前 30 天。地塞米松给药组作为阳性抗炎对照。 LPS/GalN攻击后8小时收集血清、肠道和肝脏样本进行组织学、分子和生化分析。结果：与正常对照大鼠相比，单独LPS/GalN攻击导致内毒素、肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和一氧化氮的产生显着增加。用干酪乳杆菌进行预处理不仅减少了这些变化，而且通过改善组织学评估、降低肝脏中髓过氧化物酶活性以及减少 IL-1β 和诱导型一氧化氮合酶的表达来减轻肝脏炎症。补充干酪乳杆菌可显着抑制 LPS/GalN 触发的 ERK、JNK 和 p-38 MAPK 磷酸化，但增加 TLR2、TLR9 和 PPAR-γ 的表达。此外，干酪乳杆菌张治疗通过增加粪便乳酸菌和双歧杆菌水平来预防肠道损伤并调节肠道生态。 结论：益生菌干酪乳杆菌张通过调节 TLR-MAPK-PPAR-γ 信号通路和肠道，减少 LPS/GalN 诱导的促炎细胞因子和肝脏炎症。 微生物群。
Purpose:In this study, we sought to find the effects and mechanisms of probiotic Lactobacillus casei Zhang (L. casei Zhang) on the pro-inflammatory cytokine production and hepatic inflammatory response in a rat model of acute liver failure induced by lipopolysaccharide (LPS) and d-galactosamine (GalN).Methods:Male Wistar rats were orally administrated with or without L. casei Zhang for 30 days prior to challenge with LPS and GalN. Dexamethasone administrated group serving as a positive anti-inflammation control. Serum, intestinal and liver samples were collected 8 h after LPS/GalN challenge for histological, molecular and biochemical analysis.Results:LPS/GalN challenge alone resulted in significantly increased production of endotoxin, tumor necrosis factor-α (TNF-α), interleukin-1 beta (IL-1β) and nitric oxide as compared to the normal control rats. Pretreatment with L. casei Zhang not only reduced these changes, but also attenuated hepatic inflammation as shown by improved histological assessment, decreased myeloperoxidase activity and reduced expression of IL-1β and inducible nitric oxide synthase in the liver. L. casei Zhang supplementation significantly inhibited LPS/GalN-triggered phosphorylation of ERK, JNK and p-38 MAPK, but increased the expression of TLR2, TLR9 and PPAR-γ. Moreover, L. casei Zhang treatment prevented intestinal injury and modulated the intestinal ecology by increasing the fecal Lactobacillus and Bifidobacterium levels.Conclusions:Probiotic L. casei Zhang reduces LPS/GalN-induced pro-inflammatory cytokine and hepatic inflammation through modulating the TLR-MAPK-PPAR-γ signaling pathways and intestinal microbiota.