Jasim Samer Tariq, Al-Kuraishy Hayder M, Al-Gareeb Ali Ismail
Cancer and Genetic Research, Medicine and Therapeutic, Al-Mustansiriya University, Baghdad, Iraq.
Department of Clinical Pharmacology, Medicine and Therapeutic, Al-Mustansiriya University, Baghdad, Iraq.
J Pak Med Assoc. 2019 Aug;69(Suppl 3)(8):S103-S107.
To evaluate the cardio-protective effect of Ginkgo Biloba (GB) on doxorubicin induced-cardiotoxicity.
The experimental study was conducted at the College of Medicine, Mustansiriya University, Baghdad, Iraq, from January to March, 2016, and comprised thirty Wistar Sprague male rats aged 3-4 months and weighing 200-400 g. The rats were divided into three equal groups (n=10); Group І (control): rats were treated with distilled water, Group ІІ (doxorubicin): rats were treated with distilled water and doxorubicin 20 mg/kg, and Group ІІІ (GB): rats were treated with GB and doxorubicin 20mg/kg. Serum malondialdehyde (MDA), glutathione reductase (GSH), lipid peroxidise (LPO), tumour necrosis factor-alpha (TNF-α), cardiac troponin (cTnI), brain natriuretic peptide (BNP) and caspase-3 (Cas-3) were measured using enzyme-linked immunosorbent assay kits. SPSS 20 was used to compare the effect GB with doxorubicin on the biomarkers of doxorubicin induced-cardiotoxicity.
Doxorubicin led to cardiotoxicity through elevation of cTnI, BNP, Cas-3 and LPO compared with controls (p<0.01).Also, MDA and TNF-α were elevated while; GSH was decreased significantly (p<0.01) compared with controls. Co-administration of GB with doxorubicin led to significant reduction in cTnI, Cas-3 sera levels with elevation in GSH serum level significantly (p<0.05). The effect of GB on BNP, LPO, MDA and TNF-α was insignificant (p>0.05) compared with the doxorubicin.
GB has significant cardio-protective effect through attenuation of oxidative stress during doxorubicin induced-cardiotoxicity in rats.
评估银杏叶(GB)对阿霉素诱导的心脏毒性的心脏保护作用。
实验研究于2016年1月至3月在伊拉克巴格达穆斯坦西里亚大学医学院进行,包括30只3 - 4个月大、体重200 - 400克的Wistar Sprague雄性大鼠。大鼠被分为三组,每组10只;第一组(对照组):大鼠用蒸馏水治疗;第二组(阿霉素组):大鼠用蒸馏水和20毫克/千克阿霉素治疗;第三组(GB组):大鼠用GB和20毫克/千克阿霉素治疗。使用酶联免疫吸附测定试剂盒测量血清丙二醛(MDA)、谷胱甘肽还原酶(GSH)、脂质过氧化(LPO)、肿瘤坏死因子-α(TNF-α)、心肌肌钙蛋白(cTnI)、脑钠肽(BNP)和半胱天冬酶-3(Cas-3)。使用SPSS 20比较GB与阿霉素对阿霉素诱导的心脏毒性生物标志物的影响。
与对照组相比,阿霉素通过升高cTnI、BNP、Cas-3和LPO导致心脏毒性(p<0.01)。此外,MDA和TNF-α升高,而GSH与对照组相比显著降低(p<0.01)。GB与阿霉素联合给药导致cTnI、Cas-3血清水平显著降低,GSH血清水平显著升高(p<0.05)。与阿霉素相比,GB对BNP、LPO、MDA和TNF-α的影响不显著(p>0.05)。
GB在大鼠阿霉素诱导的心脏毒性过程中通过减轻氧化应激具有显著的心脏保护作用。