复方竹节参颗粒对缩宫素诱导的原发性痛经的影响

目的探讨复方竹节参颗粒对缩宫素诱导的原发性痛经的影响。方法将KM小鼠、SD大鼠分别随机分为空白组、模型组、痛经宝阳性对照组(小鼠4.11 g/kg、大鼠1.87 g/kg)、复方竹节参颗粒组[低剂量组(小鼠6.17 g/kg、大鼠2.80 g/kg),高剂量组(小鼠18.5 g/kg、大鼠8.41 g/kg)],采用己烯雌酚(小鼠10~20 mg/kg,大鼠5~10 mg/kg)和缩宫素(小鼠20 U/kg,大鼠10 U/kg)诱导原发痛经动物模型,观察记录各组鼠的痛经表观指标(行为反应、饮食、精神状态、毛色、被毛光泽度)并进行评分,采用扭体法观察各组鼠的扭体潜伏期、扭体次数,检测给组鼠血清生化指标(PGE2、NO、MDA)水平。取己烯雌酚诱导后的大鼠子宫,离体加入缩宫素(5 U/L),15 min后加入复方竹节参颗粒(90、270 mg/L),采用PowerLab生物信号记录系统记录体外子宫平滑肌收缩张力曲线,计算收缩张力抑制率。结果与模型组比较,复方竹节参颗粒低剂量(常规剂量)组能延长扭体潜伏期,减少扭体次数(P<0.01),升高PGE2、NO水平(P<0.01),降低MDA水平(P<0.01),提高子宫平滑肌收缩张力抑制率(P<0.01)。结论复方竹节参颗粒具有较好的抗痛经作用,并且在常规剂量使用时疗效更好,可为客观评价其药效作用提供了科学依据。

熊胆粉解酒防醉作用及对急性酒精性肝损伤的保护机制

目的:探索熊胆粉防醉、解酒作用及其对急性酒精性肝损伤的保护作用机制。方法:40只小鼠随机分为模型组,阳性药组(美他多辛300 mg/kg),熊胆粉低(200 mg/kg)、高(600 mg/kg)剂量组,各10只,分别在给药前后30 min给予15 mL/kg白酒,观察熊胆粉解酒、抗醉效果(醉酒潜伏时间和睡眠时间);60只小鼠随机分为空白组,模型组,阳性药组(美他多辛300 mg/kg),熊胆粉低(200 mg/kg)、高(600 mg/kg)剂量组,各12只,连续给予除空白组外的其他组15 mL/kg白酒14 d,建立急性酒精性肝损伤模型,检测各组小鼠的肝脏系数,肝组织中乙醇脱氢酶(ADH)、乙醛脱氢酶(ALDH)、还原型谷胱甘肽(GSH)、丙二醛(MDA)的含量及超氧化物歧化酶(SOD)的含量,血清中谷丙转氨酶(ALT)、谷草转氨酶(AST)、碱性磷酸酶(AKP)、总胆固醇(TC)的含量,HE染色观察小鼠肝脏的病理变化。结果:与模型组比较,各给药组醉酒潜伏时间显著延长、睡眠时间显著减少(P<0.01);肝脏系数显著降低(P<0.05,P<0.01),肝组织中ADH、ALDH、GSH含量及SOD含量显著升高(P<0.01,P<0.05),MDA含量显著降低(P<0.01),血清中ALT、AST、AKP及TC的含量显著降低(P<0.01),肝细胞病变程度显著减轻,肝细胞形态基本恢复正常状态。结论:熊胆粉具有良好的防醉、解酒效果,对急性酒精性肝损伤亦有良好的保护作用。

Dandelion polyphenols protect against acetaminophen-induced hepatotoxicity in mice via activation of the Nrf-2/HO-1 pathway and inhibition of the JNK signaling pathway

We investigated the liver protective activity of dandelion polyphenols(DP)against acetaminophen(APAP;Paracetamol)-induced hepatotoxicity.Mice were acclimated for 1 week and randomly divided into the following groups(n=9 per group):Control,APAP,APAP+DP(100 mg·kg^–1),APAP+DP(200 mg·kg^–1),and APAP+DP(400 mg·kg^–1)groups.Mice were pretreated with DP(100,200,and 400 mg·kg^–1)by oral gavage for 7 d before being treated with 350 mg·kg^–1 APAP for 24 h to induced hepatotoxicity.Severe liver injury was observed,and hepatotoxicity was analyzed after 24 h by evaluation of biochemical markers,protein expressions levels,and liver histopathology.Pretreatment with DP was able to restore serum liver characteristics(aspartate transaminase,AST;alanine aminotransferase,ALT;alkaline phosphatase,AKP),improve redox imbalance(superoxide dismutase,SOD;glutathione,GSH;malondialdehyde,MDA),and decrease inflammatory factors(tumor necrosis factor-α,TNF-α;interleukin-1β,IL-1β).Pretreatment with DP also significantly inhibited the expression levels of nitric oxide synthase(iNOS)and cyclooxygenase-2(COX-2).Furthermore,DP pretreatment could inhibit the apoptosis of liver cells caused by APAP through up-regulation of Bcl-2 and down-regulation of Bax and caspase-9 protein.DP also down-regulated p-JNK protein expression levels to inhibit APAP-induced mitochondrial oxidative stress and up-regulated the expression of Nrf-2 and its target gene HO-1.The histopathological staining demonstrated that DP pretreatment could inhibit APAP-induced hepatocyte infiltration,congestion,and necrosis.Our results demonstrate that DP pretreatment could protect against APAP-induced hepatic injury by activating the Nrf-2/HO-1 pathway and inhibition of the intrinsic apoptosis pathway.