黄芩苷的心脑血管作用研究进展

黄芩苷是黄芩的有效成分之一,具有清除氧自由基、减轻组织的缺血再灌注损伤、扩张血管、保护心肌细胞、抗心律失常等多方面作用。本文就黄芩苷的心脑血管药理作用作一综述。     

黄芩素和黄芩苷的药理作用及机制研究进展

黄芩在我国药用历史悠久,黄芩素和黄芩苷是黄芩发挥功效的主要活性成分。黄芩素和黄芩苷具有抗菌抗病毒、清除氧自由基、抗氧化、解热、镇痛、抗炎、抗肿瘤、保护心脑血管及神经元、保肝、预防或治疗糖尿病及其并发症等作用,本文对黄芩素和黄芩苷的药理作用及作用机制的研究进展进行综述。     

黄芩苷药理作用研究进展

根据近年来已发表的有关黄芩苷的文献,介绍黄芩苷药理作用研究进展。其主要有抗肿瘤,抗病原体,对肝、脑损伤的修复保护,对糖尿病肾病的改善和抗过敏等作用。     

黄芩苷对阿霉素引起的脂质过氧化损伤的保护作用

黄芩苷是常用传统中药,它含有丰富的黄酮类化合物,其中主要是黄芩苷。黄芩苷具有广泛的药理作用,国内临床上主要用于消炎和抗感染。黄芩苷（ｂａｉｃａｌｉｎ,Ｂａｉ）能够清除羟基自由基和超氧阴离子自由基,对Ｈ２Ｏ２造成的红细胞溶血及膜流动性的降低有很好的保护...     

黄芩苷药理作用研究进展

目的：介绍黄芩苷药理作用的研究现状。方法：通过查阅文献,综述黄芩苷的药理作用。结果：黄芩苷具有对Ｃａ＾２＋的作用、清除自由基、治疗糖尿病慢性并发症和银屑病、抗ＨＩＶ和抗肿瘤等多种药理作用。结论：黄芩苷有良好的发展前途。     

黄芩化学成分及黄芩苷提取方法研究进展

黄芩为唇形科(labiatae)植物黄芩(Scutellaria baicalensis Georgi)的干燥根.黄芩及其有效成分黄芩苷、黄芩苷元、汉黄芩素和汉黄芩苷等黄酮类化合物具有抗氧化、抗炎、抗变态、抗菌、抗病毒以及抗肿瘤等广泛药理作用[1].本文将近年来黄芩化学成分及黄芩苷提取方法的研究进展作一综述.     

黄芩苷防治中枢神经系统疾病的研究进展

摘 要黄芩苷作为传统中药黄芩的有效成分,具有多种药理作用。近年来,黄芩苷在防治中枢神经系统疾病方面取得了较为丰富的成果和较大的进展,涉及的疾病包括缺血性脑损伤、出血性脑损伤、帕金森及脊髓损伤等。研究表明,黄芩苷可以抗自由基损伤、抑制神经细胞凋亡、抑制炎症因子表达、保护线粒体能量代谢、抑制凝血酶受体、调节兴奋性与抑制性氨基酸的平衡等。基于黄芩苷对中枢神经系统的保护作用,故其可能作为治疗相关疾病的潜在药物。     

黄芩苷药理作用研究新进展

目的介绍黄芩苷药理作用研究新进展。方法根据发表的相关黄芩苷的文献进行综述。结果黄芩苷除了传统的镇静、降压、清除自由基、抗心律失常等作用外,还发现其具有抗肺炎衣原体所致的动脉粥样硬化作用,对缺血再灌注损伤的大脑和心肌具有保护作用,对不同原因引起的肝损伤具有保护作用,能显著促进成纤维细胞增殖,对人牙周膜成纤维细胞具有保护作用,在体外对某些寄生虫均有明显的抑制和杀灭作用。结论黄芩苷的开发利用主要是应用其抗炎、降压等活性,对其他药理活性的研究利用相对较少;黄芩苷还具有广泛的药理活性,如缺血再灌注损伤的保护作用、肝损伤的保护作用等,有着广泛的开发与应用前景。     

野黄芩苷及其衍生物的脑靶向神经保护作用

目的 研究野黄芩苷及其衍生物的神经保护作用和脑靶向性.方法 利用体外大鼠大脑皮层神经细胞存活影响实验测定野黄芩苷及其衍生物的脑神经保护的活性,建立原代脑微血管内皮细胞和星形胶质细胞共培养的体外血脑屏障模型来评价三者的脑靶向性.结果 野黄芩苷及其衍生物均具有脑神经保护作用,野黄芩苷乙酯透过体外血脑屏障的能力强于野黄芩苷及其苷元.结论 野黄芩苷乙酯能通过血脑屏障,具有脑靶向性.     

黄芩及其有效成分的药理学研究进展

综述了黄芩及其有效成分黄芩苷、黄芩苷元、汉黄芩素、汉黄芩苷、黄芩新素Ⅰ和黄芩新素Ⅱ等黄酮类化合物的抗氧化、抗炎、抗变态、抗菌、抗病毒以及抗肿瘤等药理作用。     

黄芩苷对链脲佐菌素诱导的糖尿病模型大鼠血糖和血脂及腺苷酸活化蛋白激酶的影响

目的探讨黄芩苷对糖尿病大鼠血糖和血脂的影响及其作用机制。方法以高脂饲料(HFD)喂养雄性SD大鼠6周后,尾静脉iv给予链脲佐菌素(STZ)诱导2型糖尿病模型。黄芩苷组大鼠每天ip给予黄芩苷80 mg.kg-1,连续6周。给药0,3和6周时观察血糖、血总胆固醇(TC)、血三酰甘油(TG);给药6周时测定肝TC和丙二醛(MDA)水平;Western印迹法分析肝和骨骼肌磷酸化腺苷酸活化蛋白激酶(AMPK)及其下游靶蛋白乙酰辅酶A羧化酶(ACC)磷酸化水平。MTT法检测黄芩苷1～50μmol.L-1作用HepG2细胞24 h的细胞存活力;Western印迹法观察黄芩苷对AMPK活性的影响。结果黄芩苷80 mg.kg-1可明显降低糖尿病大鼠的血糖和血TC(P<0.05);黄芩苷可明显降低糖尿病大鼠肝TC和MDA水平(P<0.05)。糖尿病模型大鼠肝和骨骼肌磷酸化AMPK和磷酸化ACC的水平显著降低(P<0.01),而黄芩苷能激活AMPK,明显增加糖尿病大鼠肝和骨骼肌AMPK和ACC的磷酸化水平(P<0.01)。黄芩苷1和5μmol.L-1无细胞毒性,但能显著增加HepG2肝细胞磷酸化AMPK水平(P<0.01)。结论黄芩苷对糖尿病大鼠具有一定的保护作用,其作用机制可能与激活肝和骨骼肌AMPK有关。     

Protective effect of baicalin against lipopolysaccharide/D-galactosamine-induced liver injury in mice by up-regulation of heme oxygenase-1

Baicalin, a traditional anti-inflammatory drug, has been found to protect against liver injury in several experimental animal hepatitis models; however, the mechanisms underlying the hepatoprotective properties of baicalin are poorly understood. In the present study,we investigated the effects of baicalin on the acute liver injury in mice induced by Lipopolysaccharide/D-galactosamine (LPS/D-GalN). Baicalin (50, 150, and 300 mg/kg) was pretreated intraperitoneally (i.p.) at 2, 24, and 48 h respectively before LPS/D-GalN injected in mice.The mortality, hepatic tissue histology, hepatic tissue Tumor necrosis factor-alpha (TNF-alpha) and myeloperoxidase (MPO), plasma levels of TNF-alpha and alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed. Besides, western blotting analyses of nuclear factor kappa B (NF-kappaB) translocation and Heme oxygenase-1(HO-1) protein expression, as well as HO-1 activity were determined. The results showed that baicalin protected against LPS/D-GalN-induced liver injury, including dose-dependent alleviation of mortality and hepatic pathological damage, decrease of ALT/AST release and the rise of MPO. Baicalin reduced nuclear translocation of NF-kappa B, TNF-alpha mRNA and protein levels in hepatic tissues and plasma levels of TNF-alpha induced by LPS/D-GalN. Moreover, baicalin dose-dependently increased HO-1 protein expression and activity. Further, inhibition of HO-1 activity significantly reversed the protective effect of baicalin against LPS/D-GalN-induced liver injury. These results suggest that baicalin can effectively prevent LPS/D-GalN-induced liver injury by inhibition of NF-kappa B activity to reduce TNF-alpha production and the underlying mechanism may be related to up-regulation of HO-1 protein and activity.     

A novel therapeutic regimen for hepatic fibrosis using the combination of mesenchymal stem cells and baicalin

Baicalin, isolated from the root of Scutellaria baicalensis Georgi, has shown anti-inflammatory and antioxidant activities, while mesenchymal stem cells (MSCs) have the capability of self-renewal and multilineage differentiation. In the present study, we found that baicalin could promote differentiation of bone marrow-derived MSCs into hepatocytes in vitro. We then compared the therapeutic effects of five therapeutic regimens for hepatic fibrosis induced by carbon tetrachloride in vivo by analysis of serum enzymes, morphological characteristics, cytokines and cell engraftment. Transplantation of MSCs alone was able to promote partial recovery of liver function and suppression of liver inflammation, but showed little effect on reducing the fibrotic area; transplantation with baicalin-treated MSCs gave an improved therapeutic effect; MSC transplantation and baicalin administration showed a synergistic effect; transplantation with baicalin-treated MSCs in combination with baicalin administration had the best therapeutic effect for hepatic fibrosis. Therefore, we conclude that transplantation of pre-differentiated MSC together with baicalin administration may serve as an effective therapeutic regimen for severe liver diseases.     

黄芩苷对卡介苗加脂多糖诱导免疫性肝损伤小鼠的作用

目的　研究黄芩苷对免疫性肝损伤小鼠的作用。方法　采用卡介苗加脂多糖 (BCG+LPS)诱导小鼠免疫性肝损伤模型,通过检测血清谷丙转氨酶(ALT)的活性,计算脾脏等脏器指数并检查肝组织的病理损伤程度,研究黄芩苷的护肝作用。结果　黄芩苷对BCG+LPS诱导的小鼠免疫性肝损伤有明显保护作用,可降低肝损伤小鼠血清ALT的活性和肝脏、胸腺指数,与模型对照组比较有显著差异(P<0. 05~0. 01),且可不同程度减轻肝脏病理损伤。结论　黄芩苷对小鼠免疫性肝损伤有保护作用,对小鼠的免疫功能有调节作用。     

Protective effect of baicalin on tert-butyl hydroperoxide-induced rat hepatotoxicity

Baicalin (BA) is a flavonoid compound purified from Scutellaria baicalensis Georgi that is used as a traditional Chinese herbal medicine. Baicalin was studied for the mechanism of its inhibitory effects on the tert-butyl hydroperoxide (t-BHP)-induced cytotoxicity and lipid peroxidation in rat liver system. Baicalin expressed an antioxidant property by its capacity for quenching the free radicals of 1,1-diphenyl-2-picrylhydrazyl (DPPH). Further investigations using the t-BHP-induced cytotoxicity in rat primary hepatocytes demonstrated that baicalin, at the concentrations of 2–220 M, significantly decreased the leakages of lactate dehydrogenase (LDH) and alanine aminotransferase (ALT), and the formation of malondialdehyde (MDA) induced by 30 min treatment of t-BHP(1.5 mM). Baicalin also attenuated the t-BHP-induced depletion of glutathione (GSH) and high level of DNA repaired synthesis. An in vivo study in rats showed that pretreatment with baicalin (i.p.) at concentrations of 0.5 and 5 mg/kg for 5 days before a single i.p. dose of t-BHP (0.1 mmol/kg) significantly lowered the serum levels of hepatic enzyme markers (ALT and AST) and reduced oxidative stress in the liver. Histopathological evaluation of the rat livers revealed that baicalin reduced the incidence of liver lesions induced by t-BHP including hepatocyte swelling, leukocyte infiltration, and necrosis. Based on the results described above, we speculate that baicalin may play a chemopreventive role via reducing oxidative stress in living systems.     

黄芩苷化合物现代常用测定方法的分析比较

黄芩的主要有效成分黄芩苷具有抗菌消炎、解热镇痛、抗病毒、抗肿瘤、降压及利尿等作用。黄芩苷是许多复方中药制剂的主要成分,而中药成分复杂,对分析技术也有特定的要求。本文对黄芩苷测定技术分光光度法、色谱法、红外光谱分析法等进行了综述。     

葡萄籽提取物化学性保肝作用的动物试验研究

目的了解葡萄籽提取物保肝效果。方法以40、80、160mg／kg．bw剂量的葡萄籽提取物连续给大鼠灌胃30d，次日采血测定ALT及AST的含量。结果受试样品组大鼠肝匀浆的ALT、AST含量低于模型对照组。且组织病理学检察结果为阳性。结论桑叶提取物对动物具有化学性保肝的作用。     

Long-term baicalin administration ameliorates metabolic disorders and hepatic steatosis in rats given a high-fat diet

Aim:

Baicalin, one of the major flavonoids in Scutellaria baicalensis, possesses antioxidant and anti-inflammatory properties. However, the effects of baicalin on metabolic disorders and hepatic steatosis have not been investigated.

Methods:

Body weight was examined in high-fat diet (HFD)-fed rats with or without baicalin treatment. At the end of the experiment, serum biochemical parameters, liver histology and lipid profile were analyzed to assess whether the animals were suffering from metabolic disorders or hepatic steatosis. In the liver, the phosphorylation of AMP activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) and the gene expression of some enzymes involved in lipogenesis were examined. The effects of baicalin on the phosphorylation of AMPK and lipid accumulation induced by high glucose in human hepatoma HepG2 cells were also examined.

Results:

Baicalin (80 mg/kg) administered ip for 16 weeks suppressed body weight gain in HFD-fed rats. Weight reduction was accompanied by the reduction of visceral fat mass. Baicalin significantly decreased the elevated serum cholesterol, free fatty acid and insulin concentrations caused by the HFD. Baicalin also suppressed systemic inflammation by reducing the serum level of tumor necrosis factor α. Baicalin reduced hepatic lipid accumulation, enhanced the phosphorylation of AMPK and ACC and down-regulated genes involved in lipogenesis, including fatty acid synthase and its upstream regulator SREBP-1c. In HepG2 cells, baicalin (5 and 10 μmol/L) increased the phosphorylation of AMPK and decreased lipid accumulation following the addition of high glucose.

Conclusion:

Our study suggests that baicalin might have beneficial effects on the development of hepatic steatosis and obesity-related disorders by targeting the hepatic AMPK.     

Baicalin mitigated IL-1β-Induced osteoarthritis chondrocytes damage through activating mitophagy

Mitophagy is related to chondrocyte homeostasis and plays a key role in the progress of osteoarthritis (OA). Baicalin has a protective effect on OA chondrocytes, the aim of this study was to explore whether the effect of Baicalin on IL-1β-induced chondrocyte injury is related to the regulation of mitophagy. The expression of collagen II in chondrocytes was detected to identify chondrocytes. The effects of different concentrations of Baicalin (10, 20 and 40 μM), autophagy inhibitor (3-Methyladenine), autophagy activator (rapamycin) and Baicalin combined with PI3K agonist (740Y-P) on the viability (cell counting kit 8), apoptosis (flow cytometry), autophagy activation (Monodansylcadaverine staining) and mitochondrial membrane potential (JC-1 kit) of IL-1β-induced chondrocytes were evaluated. The co-localization of autophagosome and mitochondria was determined by immunofluorescence. Apoptosis-, autophagy-, PI3K/AKT/mTOR pathway- and mitophagy-related proteins were detected by western blot. Our result revealed that Baicalin and rapamycin facilitated cell viability, autophagy and mitophagy, elevated mitochondrial membrane potential and suppressed apoptosis of IL-1β-induced rat chondrocytes. In addition, Baicalin and rapamycin upregulated the levels of Bcl-2, Beclin 1, LC3-II/LC3-I, p-Drp1, PINK1 and Parkin as well as downregulated the levels of Bax, cleaved caspase-3, P62, p-PI3K/PI3K, p-mTOR/mTOR and Drp1 in IL-1β-induced rat chondrocytes. However, 3-Methyladenine did the opposite effects of Baicalin and 740Y-P reversed the effects of Baicalin on IL-1β-induced rat chondrocytes. In conclusion, Baicalin activated mitophagy in IL-1β-induced chondrocytes by inhibiting PI3K/AKT/mTOR pathway and activating PINK1/Parkin and PINK1/Drp-1 pathway, thereby reducing the chondrocyte injury.     

黄芩苷滴丸抗炎镇痛作用研究

目的 研究黄芩苷滴丸的抗炎镇痛作用,揭示其抗炎镇痛的机理,为该药的临床研究提供依据.方法 以醋酸致小鼠扭体和二甲苯致小鼠耳肿胀实验为模型,比较研究黄芩苷滴丸、黄芩苷原料药、黄芩苷固体分散体的抗炎镇痛作用.结果与结论 黄芩苷滴丸有明显的镇痛和抗炎作用,其作用优于黄芩苷原料药和黄芩苷固体分散体,且呈现良好的量效依赖关系.