Farrerol inhibits AngII-induced VSMCs proliferation by reducing Cx43 expression / 中国药理学通报

Aim To study the role of Cx43 in inhibi-tion of AngII-induced vascular smooth muscle cells(VSMCs) proliferation by farrerol. Methods The primary VSMCs were isolated and cultured by direct adherent culture methods. VSMCs were identified by immunohistochemstry. The cells were divided into the following groups:control group,AngII group,AngII+Farrerol group. The cell viability was measured by CCK-8 cell vitality test. The proliferation of VSMCs was measured by the methods of Edu. The cell cycle of VSMCs was detected by flow cytometry. The mRNA levels of Cx43 were measured by Real-time PCR. The protein levels of Cx43 were measured by Western blot. Results 60 μmol·L-1farrerol could significantly de-crease the cell viability and EdU rate of VSMCs in-duced by AngII(P<0.05),which could also prevent the transformation of VSMCs from G0/G1phase to S phase. The results of real-time PCR and Western blot showed that,compared with the model group,Farrerol could significantly reduce the mRNA and protein ex-pression level of Cx43(P <0.01). After the interfer-ence of Cx43 by siRNA, the inhibition of proliferation by farrerol decreased significantly. Conclusion Far-rerol inhibits AngII-induced VSMCs proliferation signif-icantly, which might be associated with reducing the expression of Cx43.

Vasodilation of quercetin on rat renal artery and the relationship with L-type voltage-gated Cachannels and protein kinase C / 生理学报

To investigate the diastolic function of quercetin on rat renal artery in vitro and its mechanism, the tension of rat renal artery was recorded by multi myograph system, and the L-type voltage-gated Ca channels (LVGC) current was recorded by whole-cell patch clamp technique. Quercetin produced relaxation effect on rat renal artery pre-contracted by 60 mmol/L KCl or 1 × 10 mol/L phenylephrine, and the maximal diastolic percentage was  (84.53 ± 7.35)% or (76.42 ± 4.63)%. There was no statistical difference in the maximal diastolic percentage between endothelium-intact and endothelium-denuded groups. Pre-incubation of protein kinase C (PKC) inhibitor C6303 inhibited the maximal diastolic amplitude induced by quercetin. The peak current density of LVGC in rat renal artery vascular smooth muscle cells (VSMCs) was (23.17 ± 1.33) pA/pF. Quercetin (10 μmol/L) inhibited the peak current to (10.46 ± 1.35) pA/pF, and the inhibition percentage was 54.86%. C6303 (1 μmol/L) partially reversed the inhibitory effect of quercetin, and the inhibition percentage was 62.08% (P < 0.05). These results suggest that quercetin can relax rat renal artery in vitro in a concentration-dependent and endothelium-independent manner. The vasodilation of quercetin may be related to inhibition of LVGC current and activation of PKC.