Targeting the Nrf2 signaling pathway and oxidative stress by resveratrol for Parkinson's disease: A picture...

Targeting the Nrf2 signaling pathway and oxidative stress by resveratrol for Parkinson's disease: overview and update on new developments.

Targeting Nrf2 signaling pathway and oxidative stress by resveratrol for Parkinson’s disease: an overview and update on new developments

Abstract: Parkinson's disease (PD), a prevalent neurological condition, impairs motor control functions. It is caused by the degeneration of nigrostriatal dopaminergic (DAergic) neurons. continuously Guidelines for treating Parkinson's disease At present, it is not effective because it cannot stop the progression of the disease and has side effects. Natural polyphenols, a group of phytochemicals, have been found to have many health benefits. including neuroprotection against Parkinson's disease Among these compounds, resveratrol (RES) has neuroprotective properties due to its ability to protect mitochondria and act as an antioxidant. An increase in the formation of reactive oxygen species (ROS) causes oxidative stress (OS), which causes cellular damage. This results in the oxidation of fat. Protein oxidative changes and DNA damage in Parkinson's disease models. Resveratrol has been found to reduce oxidative stress by increasing endogenous antioxidant status and directly scavenging ROS. Several studies have examined the involvement of resveratrol in modulating the transcription factor Nrf2 in Parkinson's disease models. This is because this protein recognizes oxidants and regulates antioxidant defense. In this review, we examine the molecular mechanisms underlying resveratrol's activity and review its effects in Parkinson's disease models. Both in vitro and in vivo, the evidence gathered here suggests that resveratrol therapy Provides further neuroprotection Parkinson's disease by reducing OS and upregulating Nrf2. In addition, in this study Scientific proof of its neuroprotective properties is described. Resveratrol and Parkinson's disease and mechanisms supporting consideration of clinical development.

https://link.springer.com/article/10.1007/s11033-023-08409-1

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