Chen Sihan, Zong Ying, Li Jianming, He Zhongmei, Du Rui
College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China.
College of Pharmacy, Yanbian University, Yanji 133002, China.
Nutrients. 2025 Jul 13;17(14):2306. doi: 10.3390/nu17142306.
The aim of this study was to investigate the role and potential mechanism of deer antler peptides (DAP) in D-galactose (D-gal)-induced brain injury. In the in vivo study, C57BL/6J mice were intraperitoneally injected with 400 mg/kg D-gal and gavaged with DAP (50 and 200 mg/kg) for 5 weeks. In vitro studies, D-gal (30 μg/mL) induced senescent BV2 cells were used for further research. DAP increased the expression of BDNF and VEGF in the brain tissue of aging mice, reduced the levels of oxidative stress and inflammatory factors in serum, and decreased the pathological damage of brain tissue. In vitro, DAP promoted the proliferation of D-gal-induced senescent BV2 cells, reduced ROS level, and inhibited the release of IL-1β, IL-6 and TNF-α. In addition, DAP significantly reduced the protein expressions of TLR4 and MyD88, and inhibited the phosphorylation of NF-κB. DAP can inhibit the TLR4/MyD88/NF-κB signaling pathway, reduce oxidative stress and inflammation, and promote neovascularization. This indicates the therapeutic potential of DAP as a natural bioactive substance in preventing aging-related brain injury.
本研究旨在探讨鹿茸肽（DAP）在D-半乳糖（D-gal）诱导的脑损伤中的作用及潜在机制。在体内研究中，将C57BL/6J小鼠腹腔注射400 mg/kg D-半乳糖，并灌胃给予DAP（50和200 mg/kg），持续5周。在体外研究中，使用D-半乳糖（30 μg/mL）诱导衰老的BV2细胞进行进一步研究。DAP增加了衰老小鼠脑组织中BDNF和VEGF的表达，降低了血清中氧化应激和炎症因子的水平，并减轻了脑组织的病理损伤。在体外，DAP促进了D-半乳糖诱导衰老的BV2细胞的增殖，降低了ROS水平，并抑制了IL-1β、IL-6和TNF-α的释放。此外，DAP显著降低了TLR4和MyD88的蛋白表达，并抑制了NF-κB的磷酸化。DAP可抑制TLR4/MyD88/NF-κB信号通路，减轻氧化应激和炎症反应，并促进血管新生。这表明DAP作为一种天然生物活性物质在预防衰老相关脑损伤方面具有治疗潜力。
