1.Study on the expression of ?-SMA in rats with adriamycin-induced nephrothy and intervention of Valsartan on it
Yueling DING ; Yingjun DING ; Yuyong ZHAO
Chinese Pharmacological Bulletin 1986;0(06):-
Aim To observe the changes on the expression of ?-SMA in rats with adriamycin-induced nephrothy and intervention of Valsartan. Methods The model group were made by unilateral nephrectomy with twice-adriamycin injections by caudal vein. Immunohistochemical method, flow cytometry and pathologic image analysis were used to observe the expression of ?-SMA, FN and LN in rats. Results The expression of ?-SMA was positive in the model group. Rates of positive cell and protein semi-quantitative analysis were more higher than the sham group(P
3.Effects of Compound Danshen Injection on Local Angiotensin Ⅱ in Rat kidney with Unilateral Ureteral Obstruction
Qingyou XU ; Yuyong ZHAO ; Huazhou XU ; Li ZHU ; Gang CAO ; Yanhong WEI ;
Chinese Traditional Patent Medicine 1992;0(06):-
Objective:To investigate the protective effects of Compound Danshen Injection and Benazepril on rats with obstructive nephrosis.Methods:The interstitial nephritis model of rat was established by ligating unilateral ureter. The model rats were given drug Compound Danshen Injection and Benazepril, respectively. The levels of angiotensin Ⅱ (Ang Ⅱ), endothelin (ET 1) and the activity of angiotensin converting enzyme (ACE) in renal tissues were measured. Results: The level of angiotensin Ⅱ of Compound Danshen Injection group was 42.03?13.95pg/mg lower that of pathologic group (80.19?27.31pg/mg). The level of Benazepril group was 32.53?8.07pg/mg. There were significant differences among them. The measuring results of ACE and ET 1 were similiar to that of Ang Ⅱ.Conclusion: Compound Danshen Injection and Benazepril can effectively inhibit the activity of ACE and decrease the levels of Ang Ⅱ and ET 1.
4.The genetic association between nonalcoholic fatty liver disease and type 2 diabetes mellitus in different body mass index categories: A bidirectional Mendelian randomization study
Haoxin DUAN ; Yuyong JIANG ; Tingyu WU ; Feixiang XIONG ; Yandan JIANG ; Qin ZHANG ; Saisai ZHAO ; Hao YU
Journal of Clinical Hepatology 2024;40(10):1992-1999
ObjectiveTo investigate the genetic association between nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes mellitus (T2DM) using bidirectional two-sample Mendelian randomization (MR), as well as the causal relationship between NAFLD and T2DM across different body mass index (BMI) categories. MethodsThe data were derived from genome-wide association studies conducted in European populations, with a sample size of 32 941 cases for NAFLD, 312 646 cases for T2DM, and 681 275 cases for BMI. The univariate and multivariate MR methods were used to assess the bidirectional causal relationship between NAFLD and T2DM in the general population and across different BMI subtypes. The methods of inverse-variance weighting, MR-Egger regression, constrained maximum likelihood and model averaging, and weighted median were used to conduct the MR analysis, and MR-Pleiotropy Residual Sum and Outlier, radial MR, the MR-Egger intercept method, and the Cochrane Q test were used for sensitivity analysis. ResultsThe univariate MR analysis revealed a bidirectional causal relationship between NAFLD and T2DM in the general population (forward analysis: odds ratio [OR]=9.75, 95% confidence interval [CI]: 2.57 — 37.00, P<0.001; reverse analysis: OR=1.01, 95%CI: 1.00 — 1.01, P<0.01). After adjustment for BMI, the multivariate MR analysis showed that the causal relationship between NAFLD and T2DM remained significant in the general population (OR=33.12, 95%CI: 7.57 — 144.95, P<0.000 1). The subgroup analysis showed a causal relationship between NAFLD and T2DM across all BMI subtypes (lean subgroup: OR=12.19, 95%CI: 3.35 — 44.40, P<0.001; overweight subgroup: OR=4.30, 95%CI: 1.69 — 10.92, P<0.01; obese subgroup: OR=1.67, 95%CI: 1.14 — 2.44, P<0.01). ConclusionThis study reveals the causal relationship between NAFLD and T2DM in the general population of NAFLD and across different BMI subtypes from a genetic perspective.