Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
Gastrodin as a nephroprotective agent: Molecular docking-based modulation of oxidative stress, fibrosis, and inflammation.
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Singh Anish, Sahani Priya, Dalal Diksha, Singh Lovedeep
Аннотация
BACKGROUND: Kidney diseases are a heterogeneous group of disorders characterised by progressive structural and functional impairment of the kidneys, and homeostatic imbalance. Among these, acute kidney disease (AKD), and chronic kidney disease (CKD) are the most prevalent and clinically significant forms. Notably, the high mobility group box 1/receptor for advanced glycation end products (HMGB1/RAGE) axis activates nuclear factor kappa B (NF-κB), a pivotal transcription factor responsible for pro-inflammatory cytokine production. Additionally, transforming growth factor-β1 (TGF-β1) signaling through Sma and Mad-related protein (SMADs) and mitogen-activated protein kinases (MAPK) pathways induces extracellular matrix (ECM) accumulation, contributing to tissue fibrosis.
OBJECTIVE: To review the renoprotective potential of gastrodin and elucidate its molecular interactions involved in kidney diseases.
METHODS: Gastrodin, a bioactive phenolic glycoside derived from Gastrodia elata, was evaluated using reported pharmacological evidence and molecular docking analyses. Key signaling pathways and molecular targets involved in renal injury, including RAGE, NF-κB, TGF-β1, HMGB1, NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, and the SIRT1/Nrf2 axis, were assessed to determine the multitargeted therapeutic potential of gastrodin.
RESULTS: Several studies have demonstrated that gastrodin exerts its renoprotective effects by modulating key molecular mediators, including RAGE, NF-κB, TGF-β1, HMGB1, NLRP3 inflammasome, and the SIRT1/Nrf2 signaling axis, thereby providing a multitargeted protective mechanism against renal inflammation, oxidative stress, and fibrosis. Molecular docking analyses further demonstrate strong binding affinities of gastrodin with SIRT1 (-8.0 kcal/mol), RAGE (-7.5 kcal/mol), TGF-β1 receptor (-6.1 kcal/mol), and HMGB1 (-6.0 kcal/mol).
CONCLUSION: Collectively, these findings highlight gastrodin as a promising renoprotective agent, and mechanistic insights into its molecular interactions may inform future preclinical investigations and translational strategies in renal pharmacology.
OBJECTIVE: To review the renoprotective potential of gastrodin and elucidate its molecular interactions involved in kidney diseases.
METHODS: Gastrodin, a bioactive phenolic glycoside derived from Gastrodia elata, was evaluated using reported pharmacological evidence and molecular docking analyses. Key signaling pathways and molecular targets involved in renal injury, including RAGE, NF-κB, TGF-β1, HMGB1, NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, and the SIRT1/Nrf2 axis, were assessed to determine the multitargeted therapeutic potential of gastrodin.
RESULTS: Several studies have demonstrated that gastrodin exerts its renoprotective effects by modulating key molecular mediators, including RAGE, NF-κB, TGF-β1, HMGB1, NLRP3 inflammasome, and the SIRT1/Nrf2 signaling axis, thereby providing a multitargeted protective mechanism against renal inflammation, oxidative stress, and fibrosis. Molecular docking analyses further demonstrate strong binding affinities of gastrodin with SIRT1 (-8.0 kcal/mol), RAGE (-7.5 kcal/mol), TGF-β1 receptor (-6.1 kcal/mol), and HMGB1 (-6.0 kcal/mol).
CONCLUSION: Collectively, these findings highlight gastrodin as a promising renoprotective agent, and mechanistic insights into its molecular interactions may inform future preclinical investigations and translational strategies in renal pharmacology.