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I Kinetin Protects D-Galactose-Induced Aging Rats from Splenic Oxidative Damage

机译:I激动素保护D-半乳糖诱导的衰老大鼠免受脾脏氧化损伤

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摘要

The molecular mechanisms specifying anti-oxidative and anti-aging action of kinetin (Kn) on the splenic oxidative damage of aging rats are poorly understood. Here, the Sprague Dawley (SD) rats (Rattus norregicus) aging model was proposed by napes subcutaneous injection of D-galactose, and anti-aging group were subsequently dealt with doses of 5, 10, 20 mg/kg BW of Kn. Superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-PX), catalase (CAT), lipid peroxide (LPO), spleen indexes and histopathology were evaluated. Our results showed that Kinetin significantly decreased the MDA and LPO activity, while spleen indexes, SOD, GSH-PX and CAT were higher than aging model group; histopathological studies for spleen confirmed the rescue from the aging rats. These results demonstrate that kinetin recovers the splenic cell structure and could effectively protect the spleen cells from oxidative damage and aging
机译:尚不清楚分子动力学机制指定激动素(Kn)对衰老大鼠脾脏氧化损伤的抗氧化和抗衰老作用。在此,通过颈背皮下注射D-半乳糖,提出了Sprague Dawley(SD)大鼠(Rattus norregicus)衰老模型,随后对抗衰老组给予5、10、20 mg / kg BW的Kn剂量。评价了超氧化物歧化酶(SOD),丙二醛(MDA),谷胱甘肽过氧化物酶(GSH-PX),过氧化氢酶(CAT),脂质过氧化物(LPO),脾脏指数和组织病理学。我们的研究结果表明,激动素显着降低了MDA和LPO活性,而脾脏指数,SOD,GSH-PX和CAT则高于衰老模型组。脾的组织病理学研究证实了衰老大鼠的挽救。这些结果表明,激动素可以恢复脾脏的细胞结构,可以有效地保护脾脏细胞免受氧化损伤和衰老。

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