Abstract
Emodin is an active monomer extracted from rhubarb root, which has many biological functions, including anti-inflammation, antioxidation, anticancer, and neuroprotection. However, the protective effect of emodin on nerve injury needs to be further elucidated. The purpose of this study is to investigate the effect of emodin on the neuroprotection and the special molecular mechanism. Here, the protective activity of emodin inhibiting H2O2-induced apoptosis and neuroinflammation as well as its molecular mechanisms was examined using human neuroblastoma cells (SH-SY5Y cells). The results showed that emodin significantly enhanced cell viability, reduced cell apoptosis and LDH release. Simultaneously, emodin downregulated H2O2-induced inflammatory factors, including IL-6, NO, and TNF-α, and alleviated H2O2-induced oxidative stress and mitochondrial dysfunction in SH-SY5Y cells. In addition, emodin inhibited the activation of the PI3K/mTOR/GSK3β signaling pathway. What is more, the PI3K/mTOR/GSK3β pathway participated in the protective mechanism of emodin on H2O2-induced cell damage. Collectively, it suggests that emodin alleviates H2O2-induced apoptosis and neuroinflammation potentially by regulating the PI3K/mTOR/GSK3β signaling pathway.
Highlights
Neurodegenerative diseases mainly include Parkinson’s disease (PD), vascular dementia (VD), and Alzheimer’s disease (AD) [1]
We suggested that emodin was found to alleviate H2O2-induced apoptosis of SH-SY5Y cells
Liu et al [31] suggested that emodin inhibited the production of neurotoxin and cell apoptosis by inhibiting the activation of the AMPK signaling pathway induced by Zn2+
Summary
Neurodegenerative diseases mainly include Parkinson’s disease (PD), vascular dementia (VD), and Alzheimer’s disease (AD) [1]. The incidence of neurodegenerative diseases is increasing. By 2030, about 65.7 million people will be living with neurodegenerative diseases [2]. Neurodegenerative diseases are mainly caused by oxidative stress, mitochondrial dysfunction, toxins, and inflammation [3,4,5]. At present, based on the research on the mechanism of neurodegenerative diseases, it is proposed to protect nerve cells from degenerative changes. It is urgent to find drugs to protect nerve cells and prevent or treat neurological diseases
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