Department of Nephropathy and Immunology, The Third Central Clinical College of Tianjin Medical University, Tianjin, China.
Tianjin Key Laboratory of Extracorporeal Life Support for Critical Diseases, Artificial Cell Engineering Technology Research Center, Tianjin Institute of Hepatobiliary Disease, The Third Central Hospital of Tianjin, Tianjin, China.
BMC Complement Med Ther. 2024 Jan 30;24(1):66. doi: 10.1186/s12906-023-04323-y.
It has been found that a variety of host disease states can exacerbate intestinal inflammation, leading to disruption of intestinal barrier function. Changes in the composition of the intestine microbiota, which affect downstream metabolites in turn, ultimately react against the host.
We revealed the mechanism of berberine as an intestinal protective agent in rats with renal ischemia-reperfusion injury acute kidney injury (AKI).
HE staining was performed to evaluate the pathological changes in the colon and kidney. 16 S rRNA analysis was performed to assess the intestinal microbiota. Intestine TLR4/NF-κB expression was assessed by western blot. Q-RT-PCR was performed to detect TLR4 in intestine and IL-6 and KIM-1 gene expression in the kidney. SPSS 22.0 was used to compare the data.
Rats with AKI exhibited increased relative abundances of Proteobacteria and Bacteroidetes and decreased relative abundances of Lactobacillus, Ruminococcus and Lachnospiraceae belonging to the phylum Firmicutes. The Sirt1-NF-κB-TLR4 pathway was involved in the occurrence process, accompanied by intestinal inflammation and oxidation. Berberine reversed the appeal change.
Berberine inhibits the intestinal biological barrier of Proteobacteria, reduces LPS production, exerts an anti-inflammatory effect, and delays the progression of AKI.
已发现多种宿主疾病状态可加重肠道炎症，导致肠道屏障功能紊乱。肠道微生物群落组成的改变，进而影响下游代谢物，最终对宿主产生反应。
本研究旨在揭示小檗碱作为肾缺血再灌注损伤急性肾损伤（AKI）大鼠肠道保护剂的作用机制。
采用 HE 染色评估结肠和肾脏的病理变化。采用 16S rRNA 分析评估肠道微生物群。采用 Western blot 评估肠道 TLR4/NF-κB 表达。采用 Q-RT-PCR 检测肠道 TLR4 及肾脏中 IL-6 和 KIM-1 基因表达。采用 SPSS 22.0 比较数据。
AKI 大鼠中厚壁菌门和拟杆菌门的相对丰度增加，而属于厚壁菌门的乳杆菌属、瘤胃球菌属和毛螺菌科的相对丰度降低。Sirt1-NF-κB-TLR4 通路参与了发生过程，伴随着肠道炎症和氧化。小檗碱逆转了这种吸引力的变化。
小檗碱抑制了 Proteobacteria 的肠道生物屏障，减少了 LPS 的产生，发挥了抗炎作用，并延缓了 AKI 的进展。
