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牛磺酸在非酒精性脂肪性肝病大鼠模型中调节白细胞介素-17/10的表达及肠道菌群,并保护肝脏和肠黏膜。

Taurine Regulates the Expression of Interleukin -17/10 and Intestinal Flora and Protects the Liver and Intestinal Mucosa in a Nonalcoholic Fatty Liver Disease Rat Model.

作者信息

Zhu Fu-Li, Huang Ting, Lv Zi-Li, Liang Gang, Yao Zhen, Lan Lian-Cheng, Qadir Abdul, Chen Xiu-Qi, Shan Qing-Wen

机构信息

Department of Pediatrics, the First College of Clinical Medical Science, China Three Gorges University, Yichang Central People's Hospital, Yichang, Hubei, 443000, People's Republic of China.

Department of Pediatrics, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, 530021, People's Republic of China.

出版信息

Diabetes Metab Syndr Obes. 2024 Feb 9;17:675-689. doi: 10.2147/DMSO.S440978. eCollection 2024.

DOI:10.2147/DMSO.S440978
PMID:38352234
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10863462/
Abstract

PURPOSE

To investigate the intestinal inflammatory response and the abundance of intestinal bacteria in rats with high-fat diet (HFD)-induced nonalcoholic fatty liver disease (NAFLD) and assess the intervention effects of taurine (TAU).

METHODS

Forty male Sprague-Dawley rats were randomly divided into five groups: group I, normal diet and normal saline gavage; group II, normal diet and TAU gavage; group III, HFD and normal saline gavage; group IV, HFD and TAU gavage (from the 1st week); group V, HFD and TAU gavage (from the 10th week). At the end of the 16th week, all the animals were sacrificed. Body weight, liver weight, liver function, and serum lipid levels were measured. The histopathologies of the liver and ileum were observed. The mRNA and protein expression levels of interleukin 17 (IL-17) and IL-10 in the ileum were detected by reverse transcription quantitative polymerase chain reaction (qPCR) and immunohistochemistry. Three types of bacteria were detected in intestinal feces using the 16S rDNA qPCR method.

RESULTS

The ileal IL-17 level in group III was significantly higher than those in the other four groups (P < 0.01). The ileal IL-10 mRNA levels in group IV was significantly higher than those in groups III and V (P < 0.05), and IL-10 protein MOD levels in group III was significantly lower than those in the other four groups (P < 0.01). The numbers of Lactobacillus in group III were significantly lower than those in the other four groups (P < 0.01 or P < 0.05). The numbers of Bifidobacteria in groups IV and V were significantly increased compared with that in group III (P < 0.05).

CONCLUSION

TAU may down-regulate the expression of IL-17, up-regulate the expression of IL-10 and regulate the intestinal flora, and alleviate the liver and intestinal damage in rats with HFD-induced NAFLD.

摘要

目的

研究高脂饮食(HFD)诱导的非酒精性脂肪性肝病(NAFLD)大鼠的肠道炎症反应及肠道细菌丰度,并评估牛磺酸(TAU)的干预效果。

方法

将40只雄性Sprague-Dawley大鼠随机分为五组:第一组,正常饮食并灌胃生理盐水;第二组,正常饮食并灌胃TAU;第三组,高脂饮食并灌胃生理盐水;第四组,高脂饮食并从第1周开始灌胃TAU;第五组,高脂饮食并从第10周开始灌胃TAU。在第16周结束时,处死所有动物。测量体重、肝脏重量、肝功能和血脂水平。观察肝脏和回肠的组织病理学变化。通过逆转录定量聚合酶链反应(qPCR)和免疫组织化学检测回肠中白细胞介素17(IL-17)和IL-10的mRNA和蛋白表达水平。采用16S rDNA qPCR方法检测肠道粪便中的三种细菌。

结果

第三组回肠IL-17水平显著高于其他四组(P<0.01)。第四组回肠IL-10 mRNA水平显著高于第三组和第五组(P<0.05),第三组IL-10蛋白MOD水平显著低于其他四组(P<0.01)。第三组乳酸杆菌数量显著低于其他四组(P<0.01或P<0.05)。与第三组相比,第四组和第五组双歧杆菌数量显著增加(P<0.05)。

结论

TAU可能下调IL-17的表达,上调IL-10的表达并调节肠道菌群,减轻HFD诱导的NAFLD大鼠的肝脏和肠道损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/175c/10863462/c1babe8392e0/DMSO-17-675-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/175c/10863462/f530d4ef2cbf/DMSO-17-675-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/175c/10863462/0ff876e06df9/DMSO-17-675-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/175c/10863462/d11f1991c674/DMSO-17-675-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/175c/10863462/f36317d929da/DMSO-17-675-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/175c/10863462/6bca80d3bc31/DMSO-17-675-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/175c/10863462/c1babe8392e0/DMSO-17-675-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/175c/10863462/f530d4ef2cbf/DMSO-17-675-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/175c/10863462/0ff876e06df9/DMSO-17-675-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/175c/10863462/d11f1991c674/DMSO-17-675-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/175c/10863462/f36317d929da/DMSO-17-675-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/175c/10863462/6bca80d3bc31/DMSO-17-675-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/175c/10863462/c1babe8392e0/DMSO-17-675-g0006.jpg

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