Abstract: Objective To study the relationship of L-type calcium channel (Cav1.2) mediated calmodulin/calmodulin-dependent protein kinase II (CaM/CaMKII) signaling pathway with premenstrual syndrome (PMS) with liver-qi stagnation, and elucidate the Shuyu capsule intervention mechanism. Methods The PMS model rats with liver-qi stagnation were induced by bondage stimulation, and the model rat were treated with Shuyu capsule, the extract from Radix Bupleuri and Radix Paeoniae, and fluoxetine+nimodipine as positive control. The experiment were divided into six groups: normal group, model group, Shuyu group, Radix Bupleuri, Radix Paeoniae group and fluoxetine+nimodipine group. The expression level of CaM, brain-derived neurotrophic factor (BDNF) and phosphorylation level of CaMKII were detected by Western blotting. Results Compared with the normal group, the protein expression level of p-CaMK II increased and BDNF decreased significantly in hippocampus of model rats. After treating with our medication the protein expression of CaM and CaMK II phosphorylation level decreased obviously, the expression level of BDNF increased markedly (P<0.05; P<0.01). Conclusion We hypothesized that the CaM/CaMKⅡcalcium signal pathway mediated by Cav1.2 may play important role in the pathogenesis of PMS Liver-qi stagnation and maybe the molecular targets of Shuyu capsule to treatment PMS with Liver-qi stagnation.

Key words: Premenstrual syndrome, Shuyu Capsule, Radix Bupleuri extract, Radix Paeoniae extract, L-type calcium channel (Cav1.2)