RÉSUMÉ
Aim To evaluate the protective effect of α-asarone on microglials with cerebral ischemia/reperfusion injury by measuring the expression of polar transformation and related inflammatory proteins in BV2 cells in vitro and its mechanisms.Methods The cerebral ischemia/reperfusion injury BV2 cells were pretreated by α-asarone in vitro and simulated by OGD/R model.The effect of α-asarone on the viability of damaged cells in OGD/R model was determined by CCK-8; the morphological changes of cells were observed to analyze the general morphology of cells; the levels of proinflammatory factor IL-1β, IL-18 and anti-inflammatory factor IL-10, IL-4, and ROS activity secreted by BV2 cells were detected by ELISA; the protein expressions of TGF-β, TNF-α and inflammatory related protein NLRP3, caspase 1, p-NF-κB were detected by Western blot.Results The results of in vitro experiments were as follows: the activity of damaged cells in OGD/R model was significantly increased by α-asarone, with the increase of administration dose, the cells in the low, medium and high dose groups of α-asarone decreased, and the "amoeba-like" cells and the cell body were gradually became stereoscopic and full.From the results of cell morphology, it could be seen that α-asarone had a certain proliferative effect on normal cells; the release was significantly reduced of proinflammatory factor IL-1β, IL-18 and TNF-α in OGD/R injured BV2 cells pretreated with α-asarone, also increased the release of IL-10, IL-4 and TGF-β, with a dose-effect relationship, and the high dose(16 μmol·L-1)was the best; the expressions of inflammatory related protein NLRP3, caspase 1, NF-κB and ROS activity in injured cells of OGD/R model were significantly reduced after pretreatment with α-asarone.Conclusions α-asarone has a significant protective effect on cerebral ischemia/reperfusion injury, mainly by regulating ROS activity and inhibiting phosphorylation of NF-κB, in order to reduce the excessive activation of NLRP3 inflammatory corpuscles reducing the secretion of proinflammatory factor IL-1β and IL-18, promoting the secretion of anti-inflammatory factor IL-10 and IL-4, so as to protect cerebral ischemia/reperfusion injury by anti-inflammatory reaction.
RÉSUMÉ
Objective To investigate the effect of alkaline phosphatase liver / bone / kidney (ALPL) overexpression on ventricular remodeling after acute myocardial infarction (MI). Methods Thirty six 8-week-old male C57BL / 6 J mice were randomly divided into sham group(sham), MI group (MI+Adv-EGFP) and ALPL overexpression group (MI+ Adv-ALPL) with 12 mice in each group. Two weeks after MI, cardiac function of mice was detected by echocardiography, pathological changes was detected by HE staining. ALPL mRNA expression in mouse heart was detected by Real-time PCR. The levels of ALPL, α- smooth muscle actin (α-SMA),collagen I (ColI) and collagen III (ColIII) protein were detected by Western blotting. The collagen volume fraction (CVF) and the ratio of Col I / Col III were measured by polarizing method with Sirius red staining. Results Compared with MI+Adv-EGFP group, the left ventricular ejection fraction (LVEF) (%) and left ventricular fractional shortening (LVFS) (%) of the heart in MI+Adv-ALPL group were reduced significantly (P < 0. 05). Hearts in the ALPL overexpression group showed myocardial fiber broken, and disordered and fibrous scars were obvious in myocardial infarction area. The expression of ALPL and the expression of α-SMA, ColI and ColIII protein in MI+Adv-ALPL group increased significantly (P<0. 05), and the proportion of ColI / ColIII in MI+Adv-ALPL group increased significantly (P<0. 05).Compared with MI+Adv-EGFP group, the CVF and the proportion of the ratio of ColI / ColIII in the MI+Adv-ALPL group increased significantly (P<0. 05). Conclusion ALPL overexpression can promote the ventricular pathological remodeling after acute myocardial infarction in mice.