附子正丁醇、水提取物对虚寒证模型大鼠ATP酶活性及能荷的影响

目的研究附子正丁醇、水提取物对虚寒证模型大鼠三磷酸腺苷(ATP)酶活性及能荷的影响。方法将大鼠随机分为空白对照组、模型组、附子正丁醇组、附子水提物组,模型组与治疗组大鼠均予灌含生药量3.2g/mL的造模药5mL,每天1次,连续14d,空白对照组每天灌服等量的生理盐水,造模成功后,附子正丁醇和水提物组分别灌服对应的治疗药,每日1次,连续7d,治疗结束后,分光光度数法检测大鼠肝匀浆液中的ATP酶活性,高效液相法测试ATP含量及能荷的比例。结果与空白对照组相比,模型组Na+-K+-ATP酶、Ca2+-Mg2+-ATP酶活性明显降低(P<0.01);与模型组相比,附子正丁醇组Ca2+-Mg2+-ATP酶活性升高(P<0.05),附子正丁醇组Ca2+-Mg2+-ATP酶活性高于附子水提物组(P<0.05);与空白组相比,模型组ATP含量及能荷比例均降低(P<0.05);与模型组相比,附子正丁醇组能荷比例升高(P<0.05)。结论附子正丁醇和水提物能提高虚寒证大鼠的ATP酶活性及能荷的比例,有利于虚寒证大鼠物质代谢的恢复,ATP酶活性降低可能是造成虚寒模型的原因之一,但仍需后续的研究进一步确认。

Influence of aconite normal butanol and water extract on ATPase activity and energy charge in rat model of deficiency cold syndrome

Objective To investigate the influence of aconite normal butanol and water extract on the ATPase activity and the energy charge in the rat model of deficiency-cold syndrome.Methods Wistar rats were divided into four groups:blank control group(group 1),model control group(group 2),aconite normal butanol group(group 3) and aconite water extract group(group 4).The rats in the model control and treatment groups were gavaged with the molding medicine 5mL,containing the crude drug 3.2 g/mL,once daily for 14 d,while the rats in the blank control group with same amount of normal saline.The content of Na+K+ATPase,Ca2+Mg2+ATPase,ATP and energy charge from deficiency-cold syndrome rat′ s blood plasma and liver were detected by spectrophotometer.Results The activity of Na+ K+ ATPase and Ca2+Mg2+ATPase in the group 2 was obviously lower than that in the group 1(P<0.01);the activity of Ca2+Mg2+ ATPase in the group 3 was higher than that in the group 2 and 4(P<0.05).The activity of ATPase and the percentage of energy charge in the group 2 was lower than that in the group 1(P<0.05);the percentage of energy charge in the group 3 was higher than that in the group 2(P<0.05).Conclusion Aconite normal butanol and water extract can increase the activity of ATPase and the percentage of energy charge,and benefit the restoration of material metabolism in the rat model of deficiency-cold syndrome.ATPase activity reducing may be one of causes inducing the deficiency-cold syndrome model,but which still needs subsequent research for further verification.