Effects of Sijunzi decoction-containing serum on polyamine/HuR signaling pathway during IEC-6 cell proliferation / 中国药理学通报

Aim To investigate the effect of Sijunzi Decoction on mRNA and protein expression related to growth and cell cycle in polyamine/HuR signaling pathway during small intestinal epithelial cell (IEC-6) proliferation, and to explore its mechanism on intestinal mucosal injury repair. Methods Sijunzi Decoction-containing serum (SJZD) was prepared from SD rats, the expression of HuR protein in cytoplasm and nucleus was analyzed by immunofluorescence and Western blot, the mRNA level of activating transcription factor-2 (A T F - 2), JunD and cyclin dependent kinase 4 (CDK4) were determined by real-time fluorescent quantitative PCR (RT-PCR), Western blot was used to detect protein level of HuR, ATF-2, JunD and CDK4, and flow cytometry was applied to analyse cell cycle distribution. Results Compared with the control group, the mRNA and protein expression of ATF-2 and JunD decreased, while the expression of Cdk4 mRNA and protein increased in SZJD group, and the proportion of G

Effect and mechanism of leonurine on pressure overload-induced cardiac hypertrophy in rats / 中国中药杂志

To investigate the effects of leonurine(Leo) on abdominal aortic constriction(AAC)-induced cardiac hypertrophy in rats and its mechanism. A rat model of pressure overload-induced cardiac hypertrophy was established by AAC method. After 27-d intervention with high-dose(30 mg·kg~(-1)) and low-dose(15 mg·kg~(-1)) Leo or positive control drug losartan(5 mg·kg~(-1)), the cardiac function was evaluated by hemodynamic method, followed by the recording of left ventricular systolic pressure(LVSP), left ventricular end-diastolic pressure(LVESP), as well as the maximum rate of increase and decrease in left ventricular pressure(±dp/dt_(max)). The degree of left ventricular hypertrophy was assessed based on heart weight index(HWI) and left ventricular mass index(LVWI). Myocardial tissue changes and the myocardial cell diameter(MD) were measured after hematoxylin-eosin(HE) staining. The contents of angiotensin Ⅱ(AngⅡ) and angiotensin Ⅱ type 1 receptor(AT1 R) in myocardial tissue were detected by ELISA. The level of Ca~(2+) in myocardial tissue was determined by colorimetry. The protein expression levels of phospholipase C(PLC), inositol triphosphate(IP3), AngⅡ, and AT1 R were assayed by Western blot. Real-time quantitative PCR(qRT-PCR) was employed to determine the mRNA expression levels of β-myosin heavy chain(β-MHC), atrial natriuretic factor(ANF), AngⅡ, and AT1 R. Compared with the model group, Leo decreased the LVSP, LVEDP, HWI, LVWI and MD values, but increased ±dp/dt_(max) of the left ventricle. Meanwhile, it improved the pathological morphology of myocardial tissue, reduced cardiac hypertrophy, edema, and inflammatory cell infiltration, decreased the protein expression levels of PLC, IP3, AngⅡ, AT1 R, as well as the mRNA expression levels of β-MHC, ANF, AngⅡ, AT1 R, c-fos, and c-Myc in myocardial tissue. Leo inhibited AAC-induced cardiac hypertrophy possibly by influencing the RAS system.

The inhibitory effect of compound Q-l on proliferation of MH7A induced by TNF-α and its significance / 中国药理学通报

Aim To investigate the effect of compound Q-L on MH7A based on NF-KB and MAPK signaling pathways and its mechanism. Methods Human rheumatoid arthritis fibroblast synovial cell line (MH7A) was selected as the experimental object. The effect of compound Q-l on the proliferation of MH7A cells was determined by CCK-8 method. The effect of compound Q-l on the migration ability of MH7A cells was detected by Transwell assay. TNF-α solution was used as inducer, and the content of TNF-α and IL-6 in cell supernatant was determined by ELISA. The protein expressions of p65, p-p65, IκBα, P-IκBα, p38, p-p38, ERK, p-ERK, JNK and p-JNK in the cells were determined by Western blot. Results Compound Q-l at different concentrations significantly inhibited the activity of MH7A cells. Compound Q-l significantly inhibited the migration of MH7A cells. Compound Q-l significantly reduced the contents of TNF-α and IL-6 in cell supernatant. Compound Q-l could significantly down-regulate the protein expression levels of p65, p-p65, P-IκBα, p38, p-p38 induced by TNF-α, but had no marked effects on IKBCX, ERK, p-ERK, JNK and p-JNK proteins. Conclusion Compound Q-l can significantly inhibit the proliferation of MH7A cells, reduce the expression of inflammatory cytokines TNF-α and IL-6 in cell supernatant, and down-regulate the protein expressions of p65, p-p65, IKBCX, p-LKBA, p38, p-p38 induced by TNF-α. The possible mechanism of action is related to NF-κB and p38MAPK sig-naling pathways.