Preventive and Therapeutic Efficacy of Aqueous Extract of Cordyceps bassiana Spore Powder on Gentamicin- and Cisplatin-Induced Renal Cell Injury

Background: Acute kidney injury (AKI) is driven by mechanisms such as oxidative stress, inflammation, and mitochondrial dysfunction, often triggered by nephrotoxic agents like cisplatin and gentamicin, yet effective targeted therapies remain limited. Although C. bassiana shows promising renoprotective effects, its preventive and therapeutic potential in diverse AKI models, particularly from spore-derived aqueous extracts, remains insufficiently explored. Aims: This study evaluated the preventive and therapeutic efficacy of the aqueous extract of Cordyceps bassiana spore powder (AE-CBSP) against chemically induced acute kidney injury (AKI). Methodology: AE-CBSP was prepared via aqueous boiling, and its nucleosides were quantified using high-performance liquid chromatography (HPLC). Human renal proximal tubular epithelial (HK-2) cells were used to establish in vitro AKI models induced by gentamicin (GEN) and cisplatin (DDP). The cytoprotective effects of AE-CBSP (50–800 μg/mL) were assessed in preventive (pre-treatment) and therapeutic (post-treatment) paradigms utilizing Cell Counting Kit-8 viability assays. Results: HPLC analysis confirmed AE-CBSP is abundant in nucleosides, including adenosine (980.96 μg/g) and guanosine (353.96 μg/g). Cytotoxicity screening demonstrated AE-CBSP is safe for HK-2 cells up to 800 μg/mL. In the 5 mM GEN-induced AKI model, AE-CBSP exhibited significant dose-dependent protection. Specifically, pre-treatment and post-treatment with 800 μg/mL AE-CBSP significantly elevated cell viability by 14.18% and 10.86% (P<0.05), respectively. Conversely, in the 5 μM DDP-induced model, neither preventive nor therapeutic AE-CBSP administration mitigated cytotoxicity. Conclusion: AE-CBSP exerts significant preventive and therapeutic protection against GEN-induced renal tubular epithelial cell injury but lacks efficacy against DDP-induced damage. These findings suggest that the renoprotective utility of AE-CBSP depends heavily on the specific nephrotoxic mechanism, providing an in vitro pharmacological basis for developing targeted treatments for aminoglycoside-induced AKI.