Protective effects of Tinospora crispa and Tinospora cordifolia extracts against methylglyoxal-induced oxidative stress and apoptosis in hFOB 1.19 cells: ELISA-based evaluation and molecular docking insights with antioxidant enzymes

Abstract

Background Excessive production of reactive oxygen species (ROS) and advanced glycation end products (AGE) induced by methylglyoxal (MGO) contribute to oxidative stress and cellular apoptosis in osteoblasts, ultimately disrupting bone homeostasis. This study aimed to investigate the protective effects of Tinospora crispa and Tinospora cordifolia extracts against MGO-induced oxidative stress and apoptosis in hFOB 1.19 osteoblastic cells.

Methods Methanolic and aqueous extracts were evaluated for their ability to reduce intracellular ROS, caspase-3 expression, and AGE expression through ELISA based assays. Molecular docking was performed between selected bioactive compounds of these extracts and related proteins through AutoDock Vina. Statistical analyses were performed using ANOVA, followed by post-hoc tests.

Results Methanolic extracts of T. crispa (240 µg/mL) and T. cordifolia (100 µg/mL) significantly reduced intracellular ROS levels by 46.8% and 41.2%, respectively (p < 0.05). Caspase-3 expression in MGO-induced osteoblast cells was significantly decreased following treatment with T. crispa and T. cordifolia extracts, indicating anti-apoptotic effects. However, only methanolic T. cordifolia (100 µg/mL) and aqueous T. crispa at (375 µg/mL) significantly reduced intracellular AGE expression (p < 0.05), suggesting selective effects on oxidative stress pathways. Molecular docking analysis revealed strong binding affinities of key bioactive compounds particularly towards berberine with xanthine oxidase (-8.3 kcal/mol) and caspase-9 (-8.7 kcal/mol). Meanwhile, superoxide dismutase showed a strong binding affinity towards quercetin (-7.9 kcal/mol).

Conclusion These findings suggest that T. crispa and T. cordifolia extracts possess significant antioxidant and anti-apoptotic properties, making them promising therapeutic agents in mitigating MGO-induced osteoblastic damage.