The Combination of Salidroside and Hedysari Radix Polysaccharide Inhibits Mitochondrial Damage and Apoptosis via the PKC/ERK Pathway

作者：Yang, Sixia; Wang, Linshuang; Xie, Zeping; Zeng, Yi; Xiong, Qiaowu; Pei, Tingting; Wei, Dongfeng^*; Cheng, Weidong^*

来源：Evidence-based Complementary and Alternative Medicine, 2022, 2022: 9475703.

DOI：10.1155/2022/9475703

• NEURONAL CELL-LINE
• ALZHEIMERS-DISEASE
• KINASE-C
• BETA
• IMPAIRMENT
• ACTIVATION
• MEDICINE
• RECEPTOR
• BURDEN

Background. Beta-amyloid (A beta) peptide is a widely recognized pathological marker of Alzheimer's disease (AD). Salidroside and Hedysari Radix polysaccharide (HRP) were extracted from Chinese herb medicine Rhodiola rosea L and Hedysarum polybotrys Hand-Mazz, respectively. The neuroprotective effects and mechanisms of the combination of salidroside and Hedysari Radix polysaccharide (CSH) against A beta(25-35) induced neurotoxicity remain unclear. Objective. This study aims to investigate the neuroprotective effects and pharmacological mechanisms of CSH on A beta(25-35)-induced HT22 cells. Materials and Methods. HT22 cells were pretreated with various concentrations of salidroside or HRP for 24h, followed by exposed to 20 mu m A beta(25-35) in the presence of salidroside or RHP for another 24h. In a CSH protective assay, HT22 cells were pretreated with 40 mu m salidroside and 20 mu g/mL HRP for 24h. The cell viability assay, cell morphology observation, determination of mitochondrial membrane potential (MMP), reactive oxygen species (ROS), and cell apoptosis rate were performed. The mRNA expression of protein kinase C-beta (PKC beta), Bax, and Bcl-2 were measured by qRT-PCR. The protein expression levels of cleaved caspase-3, Cyt-C, PKC beta, phospho-ERK1/2, Bax, and Bcl-2 were measured by Western blot. Results. CSH treatment increased cell viability, MMP, and decreased ROS generation in A beta(25-35)-induced HT22 cells. PKC beta and Bcl-2 mRNA expression were elevated by CSH while Bax was decreased. CSH increased the protein expression levels of PKC beta, Bcl-2, and phospho-ERK1/2, and decreased those of Bax, Cyt-C, and cleaved caspase-3. Conclusions. CSH treatment have protective effects against A beta(25-35)-induced cytotoxicity through decreasing ROS levels, increasing MMP, inhibiting early apoptosis, and regulating PKC/ERK pathway in HT22 cells. CSH may be a potential therapeutic agent for treating or preventing neurodegenerative diseases.

• 单位
  南方医科大学