Mechanistic study on hesperidin improving inflammatory microenvironment after spinal cord injury through PI3K /AKT /NF-κB signaling pathway
10.19405/j.cnki.issn1000-1492.2025.09.007
- VernacularTitle:橘皮苷通过 PI3K /AKT /NF-κB 信号 通路改善脊髓损伤后炎症微环境的机制研究
- Author:
Lei Ye
1
;
Tao You
1
Author Information
1. Dept of Orthopedics，Anhui Medical University Affiliated Provincial Hospital，Hefei 230001
- Publication Type:Journal Article
- Keywords:
spinal cord injury;
hesperidin;
inflammatory microenvironment;
PI3K/AKT/NF-κB;
oxygen glucose deprivation;
PC12 neuronal cells
- From:
Acta Universitatis Medicinalis Anhui
2025;60(9):1614-1623
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the mechanism of hesperidin on hindlimb motor function in mice with spinal cord injury(SCI).
Methods:Oxygen glucose deprivation(OGD) was used to induce SCI in PC12 neuronal cells.CCK-8 assay determined the optimal hesperidin concentration(0,10,20,30,40,50,60 mmol/L) for subsequent experiments after 24 h treatment. PC12 cells were divided into Control group,OGD group and Hesperidin(30 mmol/L) + OGD groups. Hoechst staining assessed apoptosis; Western blot(WB),qPCR and immunofluorescence(IF) detected the expression of i NOS,CD206 and TNF-α. Flow cytometry measured apoptosis rates,and WB examined the impact of hesperidin on PI3K,p-PI3K,AKT,p-AKT,and NF-κB expression. Forty-five healthy male C57BL/6 mice were randomly divided into Sham group,Sci group and Hesperidin groups. Sham and Sci groups received 0. 1 mL PBS,while the Hesperidin group received 0. 1 mL hesperidin. After modeling,i NOS,CD206,and TNF-α expression levels,spinal cord cavitation,and hindlimb motor function were evaluated.
Results:Hesperidin at 10-30 mmol/L for 24 h did not significantly affect PC12 cell activity. Hoechst staining showed reduced apoptosis in PC12 cells after 24 h of 30 mmol/L hesperidin treatment. Compared to the OGD group,Hesperidin + OGD group had decreased mRNA and protein expression of inflammatory factors(i NOS and TNF-α) and increased expression of the anti-in ammatory factor(CD206). Hesperidin treatment inhibited PI3K/AKT/NF-κB pathway activation,with similar results in mouse experiments. Compared to Sci group,Hesperidin group had reduced spinal cord cavitation area and improved hindlimb motor function.
Conclusion:Hesperidin may improve hindlimb motor function in mice with SCI by downregulating the phosphorylation level of the PI3K/AKT/NF-κB pathway,inhibiting in ammatory factor release,promoting anti-inflammatory factor release,regulating the inflammatory microenvironment after SCI,and suppressing the acute inflammatory response.
- Full text:2026032715405926266橘皮苷通过PI3K_AKT_NF-κB信号通路改善脊髓损伤后炎症微环境的机制研究_叶磊.pdf
