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长春西汀可恢复创伤性脑损伤大鼠的认知和运动功能。

Vinpocetine restores cognitive and motor functions in Traumatic brain injury challenged rats.

机构信息

Department of Pharmaceutical Sciences and Technology, Maharaja Ranjit Singh Punjab Technical University, Bathinda, 151001, Punjab, India.

出版信息

Inflammopharmacology. 2022 Dec;30(6):2243-2259. doi: 10.1007/s10787-022-01059-y. Epub 2022 Oct 3.

DOI:10.1007/s10787-022-01059-y
PMID:36190686
Abstract

Traumatic brain damage is common worldwide and the treatments are not well-defined. Vinpocetine is a synthetic derivative of the vinca alkaloid vincamine and is clinically being used for various brain disorders. Here in the current study, we have investigated the neuroprotective potential of vinpocetine against traumatic brain injury. TBI was induced by the Marmarou weight drop method in rats. Brain damage was evaluated using cognitive and motor functions and the alterations in biomolecules. Injured rats were treated with different doses of vinpocetine (2.5, 5, and 10 mg/kg) for 4 weeks. Traumatic brain injury in rats produced significant deterioration of cognition and motor functions, which was accompanied by increased oxidative stress and significant alterations in brain monoamine levels as compared with the sham control group (p < 0.05). Vinpocetine alleviated TBI-induced oxidative burden, altered neurochemistry, and improved the cognitive and motor functions as compared with that of the TBI control group (p < 0.05). The observed neuroprotective potential of vinpocetine may be due to the observed antioxidant potential and its ability to restore the levels of brain neurochemicals under stressed conditions. The outcomes of the current study may help the repositioning of vinpocetine for preventing or treating traumatic brain injuries.

摘要

外伤性脑损伤在全球范围内很常见,但其治疗方法尚未明确。长春西汀是长春碱生物堿的合成衍生物,临床上用于治疗各种脑部疾病。在本研究中,我们研究了长春西汀对外伤性脑损伤的神经保护作用。通过 Marmarou 落体法在大鼠中诱导 TBI。使用认知和运动功能以及生物分子的变化来评估脑损伤。受伤的大鼠用不同剂量的长春西汀(2.5、5 和 10 mg/kg)治疗 4 周。与假手术对照组相比,大鼠外伤性脑损伤导致认知和运动功能明显恶化,氧化应激增加,脑单胺水平发生显著变化(p<0.05)。与 TBI 对照组相比,长春西汀减轻了 TBI 引起的氧化应激,改变了神经化学,改善了认知和运动功能(p<0.05)。长春西汀观察到的神经保护作用可能是由于其观察到的抗氧化潜力及其在应激条件下恢复脑神经化学物质水平的能力。本研究的结果可能有助于重新定位长春西汀,以预防或治疗外伤性脑损伤。

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