International journal of biological macromolecules · 2025
Effects of polypeptides derived from velvet antler on D-gal induced brain aging model.
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Chen Sihan, Pei Hongyan, Geng Jianan, Zong Ying, Zhao Yan, Li Jianming, He Zhongmei, Du Rui
Аннотация
AIM: We aimed to explore the protective effects and mechanism of velvet antler polypeptides (VAP) against D-galactose (D-gal)-induced aging model in vivo and in vitro.
METHODS: The mouse model of mild cognitive impairment was established by intraperitoneal injection of D-gal (400 mg/kg). After gavage of VAP (50 and 200 mg/kg) for 4 weeks, the water maze behavior test was performed. HIF - 1α and BDNF expression levels in hippocampus were detected by immunofluorescence, neuron damage was detected by HE and Nissl staining, and inflammatory factors and oxidative stress were detected by Elisa. Protein expression was detected by western blot. The aging model of HT22 cells was established in vitro by D-gal (40 mg/L), the total enzymatic hydrolysis products were fractionated, and the best peptide (VAP-III) was screened out. The effects of VAP-III (200 and 600 μg/mL) on D-gal induced apoptosis, oxidative stress and neuroinflammation were detected. Then, Nano LC-MS/MS and molecular docking were used to predict the binding activity of VAP-III to BDNF, PI3K and Akt.
RESULTS: VAP can improve D-gal-induced neuronal damage and inhibit the production of pro-inflammatory factors and oxidative stress-related products. VAP can promote the activation of BDNF/PI3K/Akt signaling pathway.
CONCLUSION: VAP may play a neuroprotective role by regulating the BDNF/PI3K/Akt signaling pathway.
METHODS: The mouse model of mild cognitive impairment was established by intraperitoneal injection of D-gal (400 mg/kg). After gavage of VAP (50 and 200 mg/kg) for 4 weeks, the water maze behavior test was performed. HIF - 1α and BDNF expression levels in hippocampus were detected by immunofluorescence, neuron damage was detected by HE and Nissl staining, and inflammatory factors and oxidative stress were detected by Elisa. Protein expression was detected by western blot. The aging model of HT22 cells was established in vitro by D-gal (40 mg/L), the total enzymatic hydrolysis products were fractionated, and the best peptide (VAP-III) was screened out. The effects of VAP-III (200 and 600 μg/mL) on D-gal induced apoptosis, oxidative stress and neuroinflammation were detected. Then, Nano LC-MS/MS and molecular docking were used to predict the binding activity of VAP-III to BDNF, PI3K and Akt.
RESULTS: VAP can improve D-gal-induced neuronal damage and inhibit the production of pro-inflammatory factors and oxidative stress-related products. VAP can promote the activation of BDNF/PI3K/Akt signaling pathway.
CONCLUSION: VAP may play a neuroprotective role by regulating the BDNF/PI3K/Akt signaling pathway.