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巴尔比杰隆通过抑制氧化应激和乙酰胆碱酯酶水平来预防东莨菪碱诱导的大鼠记忆损伤。

Barbigerone prevents scopolamine-induced memory impairment in rats by inhibiting oxidative stress and acetylcholinesterase levels.

作者信息

AlGhamdi Shareefa A, Al-Abbasi Fahad A, Alghamdi Amira M, Omer Asma B, Afzal Obaid, Altamimi Abdulmalik S A, Alamri Abdulaziz, Alzarea Sami I, Almalki Waleed Hassan, Kazmi Imran

机构信息

Department of Biochemistry, Faculty of Sciences, King Abdulaziz University, Jeddah 21589, Saudi Arabia.

Experimental Biochemistry Unit, King Fahd Medical Research Center, King Abdulaziz University, Jeddah 21589, Saudi Arabia.

出版信息

R Soc Open Sci. 2023 Apr 12;10(4):230013. doi: 10.1098/rsos.230013. eCollection 2023 Apr.

Abstract

The current study was designed for the evaluation of barbigerone on memory loss. In this experimental study, 24 Wistar rats ( = 6) were used. Control rats and scopolamine (SCOP)-treated control group rats were orally administered with 3 ml of 0.5% sodium carboxymethyl cellulose (vehicle), whereas barbigerone was (10 and 20 mg kg) administered orally to the rats from the test group. During the 14-day treatment, control group rats were given 3 ml kg day saline, and all other groups were administered SCOP (1 mg kg day, i.p.) 1 h after barbigerone p.o. treatment. The spontaneous alternation activities, learning capacities of a rat's memory were tested with Morris water maze and Y-maze. Reduced glutathione, malondialdehyde, acetylcholine esterase (AChE) and catalase (CAT) levels were measured in rat brain tissue as oxidative stress/antioxidant markers. Moreover, the levels of tumour necrosis factor, interleukin-6 (IL-6) and IL-1 were also estimated. Treatment with barbigerone in SCOP-administered rats dramatically reduced SCOP-induced neurobehavioural deficits, oxidative stress and neuroinflammatory markers, improved endogenous antioxidants, and restored AChE activity. By improving cholinergic function and reducing oxidative damage, barbigerone could mitigate the effects of SCOP-induced changes in the brain.

摘要

本研究旨在评估巴贝吉林对记忆丧失的作用。在这项实验研究中,使用了24只Wistar大鼠(每组 = 6只)。对照组大鼠和东莨菪碱(SCOP)处理的对照组大鼠口服给予3 ml 0.5%羧甲基纤维素钠(赋形剂),而试验组大鼠口服给予巴贝吉林(10和20 mg/kg)。在为期14天的治疗期间,对照组大鼠每天给予3 ml/kg生理盐水,所有其他组在巴贝吉林口服给药1小时后腹腔注射SCOP(1 mg/kg/天)。用Morris水迷宫和Y迷宫测试大鼠记忆的自发交替活动、学习能力。测定大鼠脑组织中还原型谷胱甘肽、丙二醛、乙酰胆碱酯酶(AChE)和过氧化氢酶(CAT)水平作为氧化应激/抗氧化标志物。此外,还评估了肿瘤坏死因子、白细胞介素-6(IL-6)和白细胞介素-1的水平。在给予SCOP的大鼠中,巴贝吉林治疗显著降低了SCOP诱导的神经行为缺陷、氧化应激和神经炎症标志物,改善了内源性抗氧化剂,并恢复了AChE活性。通过改善胆碱能功能和减少氧化损伤,巴贝吉林可以减轻SCOP诱导的大脑变化的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/536e/10090886/6c1baa31593e/rsos230013f01.jpg

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