Yadav N, Khandelwal S
Industrial Toxicology Research Centre, MG Marg, Lucknow-226001, India.
Hum Exp Toxicol. 2006 Oct;25(10):581-91. doi: 10.1177/096032706072455.
The therapeutic efficacy of Picroliv--a standardized extract of Picrorhiza kurroa--was investigated in male rats exposed to CdCl2 (0.5 mg/kg, sc), 5 days/week for 18 weeks. Picroliv at two doses (6 and 12 mg/kg, po) was given to the cadmium (Cd)-administered group for the last 4 weeks (i.e., weeks 15-18). The Cd altered oxidative stress indices, such as increased lipid peroxidation and membrane fluidity, reduced levels of non-protein sulphydryls (NPSHs), and Na+K+ATPase activity in the liver and kidney were found close to the control values by Picroliv treatment, suggesting its antioxidant potential. The hepatoprotective action of Picroliv was evident by its ability to lower the Cd-induced liver function parameters--the serum enzymes, such as alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transpeptidase (GGT) and lactate dehydrogenase (LDH). Bile flow and biliary Cd also increased as a result of Picroliv's choleretic property. The Cd-induced serum urea and urinary excretion of proteins, calcium (Ca), Cd and enzymes, such as N-acetyl-beta-D-glucosaminidase (NAG) and LDH, were less marked on Picroliv treatment, indicating recovery from nephrotoxicity. Organ uptake of Cd and essential metals by Cd exposure was reduced on Picroliv treatment. Cd-induced hepatic metallothionein (MT) was lowered by Picroliv, whereas renal MT was unaltered. Cd-induced hepatic damage was also minimized. However, the renal morphological changes were marginally protected by Picroliv. The 12-mg Picroliv dose was more effective than the 6-mg dose in causing amelioration of the above parameters. This study has provided clear evidence for the hepato- and renal protective efficacy of Picroliv against experimental Cd toxicity.
研究了胡黄连苷(Picroliv)——胡黄连(Picrorhiza kurroa)的标准化提取物——对每周5天、连续18周皮下注射CdCl2(0.5 mg/kg)的雄性大鼠的治疗效果。在最后4周(即第15 - 18周),给镉(Cd)处理组大鼠灌胃两种剂量(6和12 mg/kg)的胡黄连苷。Cd改变了氧化应激指标,如脂质过氧化增加和膜流动性增强,非蛋白巯基(NPSH)水平降低,而通过胡黄连苷治疗,肝和肾中的Na + K + ATP酶活性接近对照值,表明其具有抗氧化潜力。胡黄连苷的保肝作用明显,它能够降低Cd诱导的肝功能参数——血清酶,如碱性磷酸酶(ALP)、丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、γ-谷氨酰转肽酶(GGT)和乳酸脱氢酶(LDH)。由于胡黄连苷的利胆特性,胆汁流量和胆汁中的Cd也增加。经胡黄连苷治疗后,Cd诱导的血清尿素以及蛋白质、钙(Ca)、Cd和酶(如N - 乙酰 - β - D - 氨基葡萄糖苷酶(NAG)和LDH)的尿排泄量变化不明显,表明肾毒性有所恢复。经胡黄连苷治疗后,Cd暴露导致的器官对Cd和必需金属的摄取减少。胡黄连苷降低了Cd诱导的肝脏金属硫蛋白(MT)水平,而肾脏MT未改变。Cd诱导的肝脏损伤也降至最低。然而,胡黄连苷对肾脏形态变化的保护作用微乎其微。在改善上述参数方面,12 mg胡黄连苷剂量比6 mg剂量更有效。本研究为胡黄连苷对实验性Cd毒性的肝肾保护功效提供了明确证据。