ABSTRACT
Scutellaria baicalensis Georgi, locally known as HuangQin, and commonly as Baikal or Chinese skullcap, is an important herb in Chinese traditional medicine. The flavonoids from this plant are main active substances responsible for its medicinal applications. Wogonin is one such active ingredient derived from this plant. Here, we investigated the mechanism of the vasodilation effect of wogonin on isolated rat thoracic aortas. For this study, endothelium intact and endothelium removed thoracic aortic rings were prepared from rats. Using a tension transducer, the tension of the rat thoracic aortic rings was recorded. Results showed that wogonin is able to relax the endothelium-intact aortic rings, but L-NAME, indomethacin (Indo), and methylene blue (MB) could not reduce the tension in these rings. Wogonin was also able to relax endotheliumremoved rings. However, treatment with tetraethylammonium (TEA), BaCl2, glibenclamide (Gly), 4-aminopyridine (4-AP), and verapamil (Ver) had no effect on vasodilation induced by wogonin. Using wogonin to pre-treat endothelium-removed aortic rings reduced the contraction induced by K+. Pre-treatment of endothelium-removed aortic rings with wogonin markedly reduced the contraction induced by 10-6 M PE in Ca2+-free solution. It could be concluded that L-type calcium channels and intracellular Ca2+ release is inhibited by wogonin.
ABSTRACT
Aim To observe the influences of dexmen-detomidine on the spontaneous contraction of duodenal smooth muscle of rabbits in vitro and explore the mech-anisms.Methods The rabbits ( male or female ) were stunned and the duodenums were isolated .The sam-ples of duodenal segments were connected with tension transducer , which were then put into oxygen saturation Krebs-Henseleit ( K-H) solution .The influences of dex-mendetomidine on amplitude ( AM ) and frequency ( FR ) of duodenal smooth muscle were recorded by BL-420 F biological signal processing system .The cu-mulative dosing method was used to observe the differ-ent concentrations of dexmedetomidine on duodenal smooth muscle spontaneous contraction .Glibenclamide ( Gli) was added to K-H solution before dexmendeto-midine.In the calcium-free K-H solution, calcium chloride and rynodine were added before dexmendeto-midine.The mechanisms of dexmendetomidine were studied .Results ① Dexmendetomidine reduced the amplitude of spontaneous contraction of duodenal smooth muscle in rabbits in a dose-dependent manner ( P0.05 ) .② Gli ( P <0.05 ) partly abolished the inhibitory effects of dexmendetomi-dine on duodenal smooth muscle .③ Dexmendetomi-dine inhibited the contraction of duodenum smooth muscle induced by calcium chloride ( P <0.05 ) and rynodine ( P<0.05 ) application into calcium-free K-H solution.Conclusion Dexmendetomidine inhibits the spontaneous contraction of duodenal smooth muscle of rabbits in vitro.The mechanisms may be related to ac-tivating ATP sensitive potassium channels , inhibition of the extracellular calcium influx via cell membrane and intracellular calcium release via sarcoplasmic reticulum in duodenal smooth muscle .
ABSTRACT
Aim To investigate the effect of ultra low molecular weight heparin(ULMWH)to protect primarily cultured rat cortical neurons from the deleterious effects of the neurotoxicant glutamate (Glu)and explore the related mechanism.Methods Cortical neurons of fetal rats were cultured carefully in vitro and treated with 100 ?mol?L-1 Glu so that the protective effects of ULMWH were observed thoroughly. And then the viability of cortical neurons, morphological change together with the number of apoptotic neurons,and the concentration of intracellular free Ca2+([Ca2+]i)were measured by MTT assay, Hoechst33258 staining and Fura-2/AM double wavelength fluoremetry, respectively.Results Brief exposure of cultures to 100 ?mol?L-1Glu led to extensive neuronal death and rapid increase of [Ca2+]i.Pretreatment with ULMWH over the concentration range of 0.01~1 mg?L-1 significantly inhibited the Glu-induced neuronal cell death assessed by a MTT assay and the number of apoptotic nuclei, evidenced by Hoechst 33258 staining.Glu-induced elevation of[Ca2+]i was decreased by pretreatment with 1 mg?L-1 ULMWH, which was indicated by Fura-2/AM not only in assay medium containing Ca2+ but also in Ca2+-free assay medium.Conclusions Those results suggest that ULMWH protects the cultured neurons from Glu-induced neurotoxicity, which may be attributed to its alleviating intracellular free Ca2+ overload via suppressing intracellular Ca2+ release from internal stores induced by Glu.