Dioscin attenuates inflammatory injury in uric acid-induced renal tubular epithelial cells by suppression of NF-κB signaling pathway / 中国临床药理学与治疗学

AIM: To observe the effect of Dioscin treatment on NF-κB signaling pathway and cellular inflammatory injury and explore its potential mechanism in uric acid-induced mouse tubular epithelial cells (mTECs). METHODS: After 1.2 mol/L uric acid induced mTECs, Dioscin and NF-κB P65 inhibitor BAY11-7082 were given to intervene respectively. IκB-α, NF-κB P65, PP65, NLRP3, IL-1β and β-actin were detected by Western Blot, immunofluorescence staining and real-time PCR. RESULTS: Western Blot, immunofluorescence staining and real-time PCR analysis showed that expression levels of PP65, NLRP3 and IL-1β were significantly downregulated in the uric acid-induced mTECs with Dioscin and BAY11-7082 treatment. CONCLUSION: Dioscin attenuates uric acid-induced cellular inflammatory damage by suppression NF-κB signaling pathway.

Practice and reflection on the discipline co-construction in the trusteeship of a Grade Ⅲ traditional Chinese medicine with a district hospital / 中华医学科研管理杂志

Objective:The construction of public medical group is an important strategic measure to deepen the health reform in China. Taking Beijing Traditional Chinese Medicine Hospital as an example, the article introduces the measures, achievements, existing problems and possible development direction of the discipline co-construction in the entrusted district hospital.Methods:The article analyzes the measures of discipline co-construction and its implementation effect in detail.Results:It has effectively promoted the reasonable allocation of resources between " well-developed leading disciplines" and " disciplines to be nurtured" in the medical group, these disciplines entering a new rapid development phase through optimized organization and management, system construction, new research platform construction.Conclusions:" Disciplines to be nurtured" has been improved in medical service, scientific research capabilities, talent training, academic inheritance and quality of scientific research achievements, based on which, the goal of promoting the development of medical group through discipline co-construction was achieved.

Tangshen formula promotes cellular cholesterol efflux in HG-induced mTECs by suppression of TGF-β1/Smad3 pathway / 中国临床药理学与治疗学

AIM: To observe the effect of Tangshen formula (TSF) treatment on TGF-β1/Smad3 pathway and cellular cholesterol efflux and explore its potential mechanism in HG-induced mouse tubular epithelial cells (mTECs). METHODS: After 25 mmol/L high glucose induced mTECs, TSF and Smad3 inhibitor SIS3 were given to intervene respectively. The lipid content in the cells was detected by ELISA kit; TGF-β1/Smad3 pathway and PGC-1α, LXR, ABCA1, ABCG1 were detected by Western blot and real-time PCR. RESULTS: TSF diminished the levels of TC, TG, LDL-C and increased the levels of HDL-C in HG-induced mTECs. Western blot and real-time PCR analysis showed that expression levels of TGF-β1, Smad3, Collagen and Fibronectin were significantly downregulated in the HG-induced mTECs with TSF and SIS3 treatment. And PGC-1α, LXR, ABCA1, ABCG1 expression levels were significantly upregulated in the HG-induced mTECs with TSF and SIS3 treatment. CONCLUSION: TSF can promote the cellular cholesterol efflux in HG-induced mTECs vis suppression of TGF-β1/Smad3 pathway.