BackgroundThis study attempts to investigate the therapeutic effect of sinomenine on renal fibrosis and its mechanism.MethodsThe 8‐week‐old C57BL/6 male mice were randomly divided into sham group, UUO model group, UUO sinomenine group (UUO + Sino 50), UUO + sinomenine group (UUO + Sino 100), UUO + exosome group (exo), and UUO + exo‐inhibitor. The pathological changes of kidney were observed by H&E staining, the degree of renal interstitial fibrosis was detected by MASSON and Sirius red staining, and the expressions of fibrosis and autophagy markers were detected by real‐time fluorescence quantitative PCR and WB. NTA and electron microscopy were used to analyze exo secretion after sinomenine treatment.ResultsSinomenine could improve the progression of renal fibrosis without causing tissue damage including heart, lungs and liver. Sinomenine could promote autophagosome formation. It could promote the secretion of exosomes from bone marrow mesenchymal stem cells (BMSCs). Sinomine regulates the PI3K‐AKT pathway through BMSC‐exo carrying miR‐204‐5p, affecting autophagy level and alleviating the process of renal fibrosis.ConclusionOur study suggests that sinomine could improve the progression of renal fibrosis by influencing the expression of miR‐204‐5p in BMSC‐exo and regulating the PI3K‐AKT pathway.

Purpose: Our previous study showed that Er-Bai-Tang decoction (EBT) could effectively improve Parkinson’s disease (PD) patients’ quality of life, sleep, mood, and cognitive disorders, but the mechanism of EBT to treat PD was unclear. So, our study aimed to explore the mechanism of EBT to treat PD via p38 mitogen-activated protein kinases (MAPK) pathway and intestinal flora. Methods: In our study, the PD rat model was established by subcutaneously injecting 2 mg/kg/d rotenone solution, and 23.43 g/kgEBT was used to treat PD model rats. Results: Behavioral test showed that EBT could reverse the motor impairment in the PD model rats. Hematoxylin and eosin result showed that EBT could reduce the cell necrosis in the SNpc area of the PD model rats. Western blotting and real time-polymerase chain reaction showed that EBT could decrease the p38 MAPK expression in the SNpc area of the PD model rats. 16s rRNA sequencing analysis showed that EBT could improve the composition of intestinal flora in the PD model rats. Rikenellaceae at family level and Alistipes and Allobaculum at the genus level were the key species in the PD development and EBT treatment to PD. KEGG showed that EBT might change the iron uptake in PD rats. Conclusions: EBT could improve the motor symptoms and neuronal injury in the PD model rat, and its mechanism may be related to decreasing p38 MAPK pathway and improving the composition of intestinal flora.