Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Galangin protects gastric mucosa from indomethacin-induced injury via scavenging ROS and inhibition of PKC, Akt, and NF-κB protein expressions

Jingwen Gong, Yu Xie, Yinfen Tan, Hailong Li, Junqing Zhang

Key Laboratory of Tropical Translational Medicine of Ministry of Education, Hainan Provincial Key Laboratory for Research and Development of Tropical Herbs, Haikou Key Laboratory of Li Nationality Medicine, School of Pharmacy, Hainan Medical University, Haikou 571199, China;

For correspondence:-

Accepted: 21 December 2022 Published: 30 January 2023

Citation: Gong J, Xie Y, Tan Y, Li H, Zhang J. Galangin protects gastric mucosa from indomethacin-induced injury via scavenging ROS and inhibition of PKC, Akt, and NF-κB protein expressions. Trop J Pharm Res 2023; 22(1):15-22 doi: 10.4314/tjpr.v22i1.3

© 2023 The authors.
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Abstract

Purpose: To investigate the mechanism of action of galangin (GAL) against indomethacin (Indo)-induced gastric injury.

Methods: Ten micromolar GAL with 2 mM Indo or 0.5 mM L-NAME or 2 mM propargylglycine were co-administered to human gastric mucosal epithelial cells GES-1 for 24 h. Cell viability assay and reactive oxygen species (ROS) test were conducted with commercial kits. Protein expressions of constitutive and inducible nitric oxide synthase (cNOS and iNOS, respectively), and cystathionine-γ-lyase (CSE) in GSE-1 cells were investigated by western blot. After 100 - 300 mg/kg, GAL was daily administered to rats for 5 days, and 30 mg/kg Indo was administered to induce gastric injury. Protein expressions of endothelial NOS (eNOS), iNOS, CSE, nuclear factor (NF)-κB, PKC, Akt, phospho-eNOS (Ser-1177), and phospho-eNOS (Thr-495) were investigated by western blot.

Results: Galangin ameliorated the proliferative inhibitions of Indo, propargylglycine, and L-NAME on GSE-1 cells (p < 0.05), rapidly scavenged ROS, and increased cNOS protein expressions (p < 0.05). Galangin (300 mg/kg) inhibited protein expressions of iNOS (p < 0.01), NF-κB, Akt, and PKC (p < 0.05), inhibited the Ser-1177 and Thr 495 phosphorylation of eNOS, elevated eNOS and CSE protein expressions (p < 0.001).

Conclusion: Galangin protects gastric mucosa from Indo by scavenging ROS and inhibiting protein expressions of Akt and PKC. The inhibition leads to Ser-1177 and Thr 495 dephosphorylation of eNOS, thereby prolonging eNOS activity. Besides, GAL inhibits iNOS-produced NO by inhibiting NF-κB to ameliorate the inflammatory reaction induced by Indo.

Keywords: Galangin, Non-steroidal anti-inflammatory drug, cNOS, Gastric injury