Objective To investigate the effects of Jiawei Danshen Decoction on endothelial cell ultrastructure, serum NO and ET in apolipoprotein E-knockout atherosclerosis (AS) mice;To discuss its mechanism of anti-atherosclerosis.Methods Totally 24 7-8 weeks old ApoE -/- mice were fed with a high fat diet for 12 weeks until the a mature atherosclerotic plaque was formed. They were randomly divided into four groups:model group, control group,Jiawei Danshen Decoction of low-dose group and high-dose group, 6 mice in each group. Another 6 normal C57BL/6J mice with the same strain were set as the blank group, and fed with general diet. After medicine intervention by gavage for 8 weeks, blood was extracted from orbital venous to measure serum NO and ET;aortic endothelial cell ultrastructure changes were observed by transmission electron microscope.Results Compared with the blank group, the level of NO obviously decreased and ET significantly increased in the model group (P<0.01). Compared with model group, medicine intervention increased NO and reduce ET level (P<0.05). Electron microscopy results showed that the model group showed fatty streaks stage performance;endothelial damage in each administration group was improved compared with model group.Conclusion Jiawei Danshen Decoction can improve the endothelial cell ultrastructure and functions and protect endothelial cells, with a purpose to delay the AS process.

Objective To explore the effect of astilbin(astilbin-CS-NPs)-loaded chitosan nanoparticles(CS-NPs)on high glucose(HG)-induced ferroptosis of renal tubular epithelial cells via regulating mitogen-activated protein kinase 14(MAPK14)/heat shock protein 27(HSP27).Methods HK-2 cells were divided into the following groups:normal glucose(NG)group,HG group,HG+astilbin-CS-NPs(0,5,10,20 mg/L)group,and under HG condition,pcDNA3.1-MAPK14 group,pcDNA3.1-MAPK14+astilbin-CS-NP group,si-HSP27 group,pcD-NA3.1-MAPK14+si-HSP27 group,and pcDNA3.1-MAPK14+si-HSP27+astilbin-CS-NPs group.Cell viability was detected using CCK-8 assay,cell apoptosis was detected via Tunel assay.Meanwhile,iron ion levels,lactate dehydrogenase(LDH)activity,glutathione(GSH)levels,and reactive oxygen species(ROS)levels were meas-ured using assay kits.Rat model of diabetic kidney disease(DKD)was constructed and intervened with astilbin-CS-NPs to explore the effects of astilbin-CS-NPs on DKD in vivo.Results Compared with the NG group,the HK-2 cell viability in the HG group was significantly reduced,apoptosis increased,iron ion levels,LDH activity,and ROS levels were significantly elevated,while GSH levels significantly decreased(all P＜0.05).Treatment with astilbin-CS-NPs significantly reversed the effects of HG on the biological behavior of HK-2 cells and ferroptosis-re-lated indicators.Additionally,compared to the pcDNA3.1 group,the pcDNA3.1-MAPK14 group showed increased ferroptosis,which was improved by knocking down HSP27 or co-intervention with astilbin-CS-NPs.In vivo experi-mental results showed that astilbin-CS-NPs could improve DKD rat kidney injury,inhibit iron ion levels and the ex-pression of MAPK14/HSP27.Conclusion Astilbin-CS-NPs may improve HG-induced ferroptosis of renal tubular epithelial cells via inhibition of MAPK14 and HSP27 expression.

Objective:To explore the protective effect of Shen’an decoction on cisplatin induced renal injury in rats by regulating TLR4/NF-κB signaling pathway. Methods:Sixty SD rats were randomly divided into blank group, model group, positive control group, high dose Shen’an Decoction group, medium dose Shen’an Decoction group and low dose Shen’an Decoction group, with 10 rats in each group. Except the blank group, the other groups were intraperitoneally injected with cisplatin 7.5 mg/kg to prepare the acute kidney injured rat model. After the modeling, the high, medium and low dose groups of Shen’an Decoction were gavaged with 0.698, 1.395 and 2.790 g/ml Shen’an Decoction respectively, and the positive control group was gavaged with benazepril hydrochloride suspension of 5 mg/kg, once a day for 14 days. The kidney histopathological changes of rats in each group were observed by HE staining. The content of BUN, creatinine(CR), Cystatin C (Cys-C), TNF-α, and IL-6 in serum were detected by ELISA. The expression of TLR-4, NF-κB p65, myeloid differentiation factor (MyD88), and tumor necrosis factor receptor related factor 6 (TRAF-6) in renal tissue were detected by Western blot. Results:Compared with the model group, the growth condition of rats in each dose group of Shen’an Decoction was significantly improved ( P<0.05), and the kidney coefficient was significantly decreased ( P<0.05). The serum levels of BUN, Cr, Cys-C, TNF-α, IL-6 of rats in each dose group of Shen’an Decoction were significantly decreased ( P<0.05). The expression of TLR-4 (0.54 ± 0.07, 0.52 ± 0.09, 0.41 ± 0.04 vs. 0.86 ± 0.06), NF-κB (0.74 ± 0.02, 0.72 ± 0.06, 0.67 ± 0.05 vs. 0.93 ± 0.03), MyD88 (0.86 ± 0.02, 0.82 ± 0.03, 0.61 ± 0.02 vs. 1.04 ± 0.03), and TRAF-6 (0.65 ± 0.04, 0.58 ± 0.08, 0.54 ± 0.07 vs. 0.90 ± 0.06) in kidney tissue of rats in each dose group of Shen’an Decoction was significantly decreased ( P<0.05). Conclusion:Shen’an Decoction can protect the renal function of rats by inhibiting TLR4/NF-κB signaling pathway and alleviating the pathological changes of renal injury induced by cisplatin.