Exploring the effects of naringenin on cell functioning and energy synthesis in the hippocampus of male Wistar rats with chronic tinnitus, by examining genetic indicators such as Bax, Bcl-2, Tfam, and Pgc-1α

Background

The pivotal factors, including neural plasticity, oxidative stress, neuronal inflammation, and apoptosis, play a significant role in the pathogenesis of tinnitus. The balance between Bax/Bcl-2 genes is an important factor in determining the rate of apoptosis. Pgc-1α and Tfam genes are fundamental regulators of mitochondrial biogenesis. Naringenin possesses significant antioxidant, neuroprotective, anti-inflammatory, anti-apoptotic, and antiviral properties, and its compounds are effective on cell signaling pathways.

Aims

In light of the aforementioned information, we endeavored to evaluate the impact of naringenin on the expression levels of Bax, Bcl-2, Pgc-1α, and Tfam genes in the hippocampus of male Wistar rats with chronic tinnitus.

Material and Methods

To demonstrate the existence of tinnitus, all rats were instructed to complete an “active avoidance test” utilizing a conditioning box. The expression levels of genes mentioned above were assessed using real-time PCR.

Results

The sodium salicylate at a dosage of 350 mg/kg showed an upregulation in the expression level of Bax and a downregulation in the expression level of the Bcl-2 gene (p < 0.001). Furthermore, the sodium salicylate displayed significantly higher expression levels of Tfam and Pgc-1α (p < 0.001) genes. The naringenin, at a dose of 100 mg/kg, led to a decrease in Bax gene expression (p < 0.05) and an increase in Bcl-2 gene expression (p < 0.05). On the other hand, naringenin restored the expression level of both Tfam (p < 0.001) and Pgc-1α (p < 0.01) genes.

Conclusions

Our research findings demonstrate that sodium salicylate-induced tinnitus leads to enhanced apoptosis and mitochondrial biogenesis within the hippocampus. Additionally, our evidence recommends that naringenin can reduce apoptosis effectively and maintain a balanced mitochondrial state.