■在本研究中,评价了藏红花素对气管平滑肌细胞(TSM)的松弛作用及其可能的机制。
■对8组54只雄性Wistar大鼠进行研究。TSM通过乙酰甲胆碱(10μM)和KCl(60mM)收缩,以及四种累积浓度的番红花酸的松弛作用,藏红花花瓣提取物,和茶碱在非孵育和与普萘洛尔孵育的TSM上进行检查,扑尔敏,地尔硫卓,阿托品,格列本脲,和吲哚美辛进行了调查。
■在由乙酰甲胆碱或氯化钾收缩的非孵育TSM中,番红花素和茶碱表现出浓度依赖性松弛作用(所有,P<0.001)。然而,与茶碱相比,各种浓度的番红花酸显示出明显较低的松弛作用(所有,P<0.001)。在乙酰甲胆碱诱导的TSM收缩中,与普萘洛尔一起孵育的TSM中最后浓度的番红花酸的松弛作用低于未孵育的TSM(P<0.05)。在用扑尔敏孵育的TSM中,最后两个浓度的番红花素的松弛作用显着低于KCl收缩的未孵育组织(P<0.05和P<0.0)。与格列本脲一起孵育的TSM中的EC50番红花素水平,扑尔敏,和吲哚美辛明显低于未孵育的(所有,P<0.05)。
■结果表明,藏红花酸对TSM具有有效的松弛作用,并被认为是通过刺激β-肾上腺素能受体,抑制组胺(H1)受体,钾通道开放机制。
UNASSIGNED: In the present study, the relaxant effect of crocetin on tracheal smooth muscle cells (TSM) and its possible mechanisms were evaluated.
UNASSIGNED: The study was conducted on 54 male Wistar rats in 8 groups. TSM was contracted by methacholine (10 μM) and KCl (60 mM), and the relaxant effects of four cumulative concentrations of crocetin, petal extract of saffron, and theophylline were examined on non-incubated and TSM incubated with propranolol, chlorpheniramine, diltiazem, atropine, glibenclamide, and indomethacin were investigated.
UNASSIGNED: In non-incubated TSM contracted by methacholine or KCl, crocetin and theophylline showed concentration-dependent relaxant effects (all, P<0.001). However, various concentrations of crocetin showed significantly lower relaxant effects compared to those of theophylline (all, P<0.001). In the methacholine-induced contraction of TSM, the relaxation effect of the last concentration of crocetin in the TSM incubated with propranolol was lower than in non-incubated TSM (P<0.05). In the incubated TSM with chlorpheniramine, the relaxant effects of the two last concentrations of crocetin were significantly lower than in the non-incubated tissues contracted by KCl (P<0.05 and P<0.0). The levels of EC50 crocetin in the incubated TSM with glibenclamide, chlorpheniramine, and indomethacin were markedly lower than in non-incubated (all, P<0.05).
UNASSIGNED: The results showed potent relaxation effects of crocetin on TSM and were suggested to be through stimulation of ß-adrenergic receptors, inhibition of histamine (H1) receptors, and potassium channel opening mechanisms.