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The role of Nardostachys jatamansi against doxorubicin-induced toxicity in rats

机译：Natastachys jatamansi对阿霉素诱导的大鼠毒性的作用

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This investigation elucidated the role of free radicals in doxorubicin-induced toxicity and protection by Nardostachys jatamansi (NJ). Adult male albino wistar rats were administered with doxorubicin (15 mg/kg; i.p.) and NJ (500 mg/kg, orally) for seven days. At the end of the experiment, following decapitation, heart and liver tissue samples were taken for histological examination, determination of malondialdehyde (MDA), glutathione (GSH) and myeloperoxidase (MPO) activity. In addition, proinflammatory cytokine (TNF-α) was assayed in plasma samples. The results reveal that doxorubicin caused a significant decrease in GSH level, significant increases in MDA level and MPO activity. Similarly, plasma cytokine level was elevated in doxorubicin group compared with the control group. On the other hand NJ pretreatment reversed all these biochemical indices. The results demonstrate that NJ extract, by balancing the oxidant-antioxidant status and inhibiting the generation of proinflammatory cytokine, protects against doxorubicin-induced oxidative organ injury.
机译：这项研究阐明了自由基在阿霉素诱导的毒性和Nardostachys jatamansi（NJ）的保护中的作用。成年雄性白化病wistar大鼠接受阿霉素（15 mg / kg;腹腔注射）和NJ（500 mg / kg口服）服药7天。在实验结束时，在断头之后，采集心脏和肝脏组织样品进行组织学检查，丙二醛（MDA），谷胱甘肽（GSH）和髓过氧化物酶（MPO）活性的测定。另外，在血浆样品中测定促炎细胞因子（TNF-α）。结果表明，阿霉素可导致GSH水平显着下降，MDA水平和MPO活性显着增加。同样，阿霉素组血浆细胞因子水平较对照组高。另一方面，新泽西州预处理逆转了所有这些生化指标。结果表明，NJ提取物通过平衡氧化剂-抗氧化剂的状态并抑制促炎性细胞因子的产生，可以防止阿霉素诱导的氧化器官损伤。

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