Analysis of the Mechanism of Action of Naringnin on Nerve-Damaged Cells Based on Nrf2/HO-1 and NF-κβ Signaling Pathways

Objective: To explore the mechanism of action of naringin in protecting nerve-damaged cells through Nrf2/HO-1 and NF-κβ signaling pathways. Methods: In this study, primary microglia were obtained from 8 neonatal suckling mice and treated with different concentrations of naringin, including a control group (control group) and 4 experimental groups. The activity of primary microglia was assessed using the MTT assay, while apoptosis was evaluated using the TUNEL assay. Molecular biology techniques and cell biology methods were employed to study two types of neuronal cells: highly differentiated PC12 cells and primary microglia. Oxidative stress indicators such as reactive oxygen species (ROS), malondialdehyde (MDA), mitochondrial membrane potential (MMP), and glutathione peroxidase (GSH), as well as inflammatory factors including interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α), were detected. Additionally, the expression of related proteins and genes in the Nrf2 signaling pathway and the NF-κB signaling pathway was examined to elucidate the protective effect of naringnin on neuronal cells during oxidative stress and inflammation, as well as the underlying mechanism. Results: In comparison to the control group, naringin treatment resulted in a statistically significant upregulation of the gene expression of Nrf2 and HO-1 in PC12 cells (P < 0.05). Furthermore, compared to the blank control/negative control/model group, naringin notably mitigated the levels of superoxide dismutase, glutathione, malondialdehyde, and nitric oxide in the rats, along with a significant reduction in apoptosis of neurological injury cells (P < 0.05). Conclusion: Naringin boosts cellular antioxidant capacity by activating the Nrf2/HO-1 signaling pathway, thus mitigating damage to nerve cells inflicted by oxidative stress. Additionally, it reduces the release of inflammatory factors by inhibiting the NF-κB signaling pathway, thereby decreasing inflammation levels. This dual action helps safeguard neural tissues from oxidative and inflammatory damage, ensuring the maintenance of normal nerve cell function.