Dilong (Earthworm) alleviates cyclophosphamide-induced brain injury by reducing mitochondrial damage in neuronal cells

The experiment was designed to explore the effects and mechanism of Dilong on alleviating cyclophosphamide (CTX)-induced brain injury in mice. Fifty male SPF Kunming mice aged 6-8 weeks were randomly divided into five groups: Group A served as the control group; Group B received intraperitoneal injection of CTX; Groups C, D, and E were administered Dilong at doses of 100, 200, and 400 mg/kg respectively for 14 days after intraperitoneal injection of CTX. Results showed that after modeling, the movement speed of mice significantly decreased (P < 0.05), and the number of neurons in the hippocampus and cortex decreased. Dilong can mitigate the behavioral abnormalities and reduction of brain neuronal cells caused by CTX. CTX had no significant effect on the number of astrocytes, microglia, and microglia M1 and M2 polarization, but it had a significant damaging effect on neuronal cells (P < 0.05). The mechanism of action is that CTX causes a decrease in cellular mitochondrial respiratory enzyme activity (P < 0.05) and abnormal mitochondrial structure, which leads to the activation of the cellular scorching pathway. Dilong significantly increased mitochondrial respiratory enzyme activity (P < 0.05), and the mitochondrial structure was restored to some extent. By significantly reducing NLRP3/TLR4/caspase1/pro caspase1/GSDMD (P < 0.05), it increased neuronal cell survival. This resulted in an increase in neuronal cell survival, thus exerting a protective effect on the brain.