机构地区:[1]湖南省娄底市中心医院肿瘤内科,湖南娄底417000 [2]湖南省娄底市中心医院心内科,湖南娄底417000
出 处:《中国医药导报》2014年第24期25-28,共4页China Medical Herald
摘 要:目的观察丹参酮ⅡA对阿霉素所致大鼠心肌损伤的保护作用及可能机制。方法将SD大鼠随机分为对照组、模型组(阿霉素心脏损伤)、丹参酮ⅡA组(1.0×10-5、2.0×10-5、4.0×10-5 mol/L)。丹参酮ⅡA组大鼠造模前给予20 mL/kg体积丹参酮ⅡA混悬液灌胃,连续5 d,第5天给药后1 h腹腔注射18 mg/kg阿霉素溶液,此后继续灌胃2 d。检查大鼠的心脏功能,检测大鼠血浆乳酸脱氢酶(LDH)、肌酸激酶(CK)、丙二醛(MDA)、超氧化物歧化酶(SOD)水平和心肌组织中肌钙蛋白Ⅰ(cTnⅠ)水平。结果与模型组相比,丹参酮ⅡA组(2.0×10-5、4.0×10-5 mol/L)明显改善心脏功能,表现为左室收缩压[(75.14±16.08)mm Hg比(120.37±10.89)、(123.55±10.92)mm Hg,F=8.69]、左室压力差[(65.32±17.37)mm Hg比(93.94±19.52)、(103.39±15.9)mm Hg,F=9.24]、左室内压最大上升速率[(3348.82±102.17)mm Hg/s比(4933.74±188.33)、(5188.75±205.14)mm Hg/s,F=9.83]和左室内压最大下降速率[(2559.72±433.62)mm Hg/s比(3353.94±203.15)、(3699.76±179.34)mm Hg/s,F=10.81]均显著性升高(均P<0.05)。与模型组比较,丹参酮ⅡA(2.0×10-5、4.0×10-5 mol/L)显著降低了心肌组织匀浆中cTnⅠ[(1.23±0.58)ng/mgpr比(0.39±0.13)、(0.34±0.10)ng/mgpr,F=9.13]、LDH[(3460.91±656.37)U/L比(2874.11±1130.76)、(2608.12±538.25)U/L,F=8.84]、CK[(1.74±0.64)U/mL比(0.97±0.41)、(0.96±0.44)U/mL,F=8.64]和MDA[(8.34±2.86)μmol/mL比(5.19±1.92)、(5.00±1.44)μmol/mL,F=10.54]的水平,增加了SOD活性[(81.43±28.61)kU/L比(118.22±30.54)、(120.26±15.87)kU/L,F=9.68](均P<0.05)。结论丹参酮ⅡA对阿霉素诱导的大鼠心肌损伤具有保护作用,其机制可能是丹参酮ⅡA抑制氧化应激有关。Objective To investigate the protective effect of Tanshinone IIA on the cardiac injury induced by Adriamycin and explore the probalble mechanism in rats. Methods The SD rats were randomly divided into control group, model group (Adriamycin-induced cardiac injury) and TanshinoneIIA group (1.0×10-5, 2.0×10-5, 4.0×10-5 mol/L). TanshinoneIIA (20 mL/kg) was administered by lavage every day, in the fifth days, Adriamycin (18 mg/kg) was administered by intraperitoneal injection 1 hour after treatment with Tanshinone IIA. Then Tanshinone IIA was administered for 2 days. The cardiac function of rats was tested. The levels of cardiac troponinⅠ(cTnⅠ) in myocardial homogenate and plasma lactate dehydrogenase (LDH), creatine kinase (CK), malonaldehyde (MDA) and superoxide dismutase (SOD) were measured. Results Compared with the model group, the cardiac function of rats in model group was significantly improved, the left ventricular systolic pressure [(75.14±16.08) mm Hg v s (120.37±10.89), (123.55±10.92) mm Hg, F=8.69], left ventricular pressure difference [(65.32±17.37) mm Hg vs (93.94±19.52), (103.39±15.9) mm Hg, F=9.24], +dp/dtmax [(3348.82±102.17) mm Hg/s v s (4933.74±188.33), (5188.75±205.14) mm Hg/s, F=9.83] and-dp/dtmin [(2559.72±433.62) mm Hg/s v s (3353.94±203.15), (3699.76±179.34) mm Hg/s, F=10.81] were significantly increased in Tanshinone IIA (2.0×10-5, 4.0×10-5 mol/L) (all P〈0.05). Compared with the model group, the levels of cTnⅠ [(1.23±0.58) ng/mgpr v s (0.39±0.13), (0.34±0.10) ng/mgpr, F=9.13] in myocardial homogenate and plasma LDH [(3460.91±656.37) U/L v s (2874.11±1130.76), (2608.12±538.25) U/L,F=8.84], CK[(1.74±0.64) U/mL vs (0.97±0.41), (0.96±0.44) U/mL, F=8.64] and MDA [(8.34±2.86)μmol/mL v s (5.19±1.92), (5.00±1.44)μmol/mL, F=10.54] were significantly decreased (all P〈 0.05) and&amp;nbsp;the levels of plasma SOD [(8
分 类 号:R542.2[医药卫生—心血管疾病]
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