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绿茶提取物对溴氰菊酯诱导的大鼠脑氧化损伤和细胞凋亡的影响。

Influence of green tea extract on oxidative damage and apoptosis induced by deltamethrin in rat brain.

作者信息

Ogaly Hanan A, Khalaf A A, Ibrahim Marwa A, Galal Mona K, Abd-Elsalam Reham M

机构信息

Department of Biochemistry and Chemistry of Nutrition, Faculty of Veterinary Medicine, Cairo University, Giza, Egypt.

Department of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, Cairo University, Giza, Egypt.

出版信息

Neurotoxicol Teratol. 2015 Jul-Aug;50:23-31. doi: 10.1016/j.ntt.2015.05.005. Epub 2015 May 23.

Abstract

In the present study, we investigated the protective effect of an aqueous extract of green tea leaves (GTE) against neurotoxicity and oxidative damage induced by deltamethrin (DM) in male rats. Four different groups of rats were used: the 1st group was the vehicle treated control group, the 2nd group received DM (0.6 mg/kg BW), the 3rd group received DM plus GTE, and the 4th received GTE alone (25 mg/kg BW). The brain tissues were collected at the end of the experimental regimen for subsequent investigation. Rats that were given DM had a highly significant elevation in MDA content, nitric oxide concentration, DNA fragmentation and expression level of apoptotic genes, TP53 and COX2. Additionally, a significant reduction in the total antioxidant capacity in the second group was detected. The findings for the 3rd group highlight the efficacy of GTE as a neuro-protectant in DM-induced neurotoxicity through improving the oxidative status and DNA fragmentation as well as suppressing the expression of the TP53 and COX2 genes. In conclusion, GTE, at a concentration of 25mg/kg/day, protected against DM-induced neurotoxicity through its antioxidant and antiapoptotic influence; therefore, it can be used as a protective natural product against DM-induced neurotoxicity.

摘要

在本研究中,我们调查了绿茶水提取物(GTE)对溴氰菊酯(DM)诱导的雄性大鼠神经毒性和氧化损伤的保护作用。使用了四组不同的大鼠:第一组为溶剂处理对照组,第二组接受DM(0.6 mg/kg体重),第三组接受DM加GTE,第四组单独接受GTE(25 mg/kg体重)。在实验方案结束时收集脑组织用于后续研究。给予DM的大鼠丙二醛(MDA)含量、一氧化氮浓度、DNA片段化以及凋亡基因TP53和COX2的表达水平显著升高。此外,检测到第二组的总抗氧化能力显著降低。第三组的研究结果突出了GTE作为神经保护剂在DM诱导的神经毒性中的功效,其通过改善氧化状态和DNA片段化以及抑制TP53和COX2基因的表达来实现。总之,浓度为25mg/kg/天的GTE通过其抗氧化和抗凋亡作用保护大鼠免受DM诱导的神经毒性;因此,它可以用作预防DM诱导的神经毒性的天然保护产品。

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