Abstract
Globally, gastric ulcer is a vital health hazard for a human. Rabdosia inflexa (RI) has been used in traditional medicine for inflammatory diseases. The present study aimed to investigate the protective effect and related molecular mechanism of RI using lipopolysaccharide (LPS)-induced inflammation in RAW 246.7 cells and HCl/EtOH-induced gastric ulcer in mice. We applied 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), nitric oxide (NO), reactive oxygen species (ROS), histopathology, malondialdehyde (MDA), quantitative real-time polymerase chain reaction (qPCR), immunohistochemistry (IHC), and Western blot analyses to evaluate the protective role of RI. Study revealed that RI effectively attenuated LPS-promoted NO and ROS production in RAW 246.7 cells. In addition, RI mitigated gastric oxidative stress by inhibiting lipid peroxidation, elevating NO, and decreasing gastric inflammation. RI significantly halted elevated gene expression of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), inducible nitric oxide synthetase (iNOS), and cyclooxygenase-2 (COX-2) in gastric tissue. Likewise, RI markedly attenuated the mitogen-activated protein kinases (MAPKs) phosphorylation, COX-2 expression, phosphorylation and degradation of inhibitor kappa B (IκBα) and activation of nuclear factor kappa B (NF-κB). Thus, experimental findings suggested that the anti-inflammatory and gastroprotective activities of RI might contribute to regulating pro-inflammatory cytokines and MAPK/NF-κB signaling pathways.
Highlights
Alcohol consumption is a recognized risk factor for human health
Ethanol is absorbed through the intestinal wall and metabolized in the liver in different ways: oxidation by alcohol dehydrogenase (ADH), cytochrome P450 2E1 (CYP2E1), and catalase enzymes
Oxidative stress plays a crucial role in the pathogenesis of alcoholic tissue damage and increases lipid peroxidation, which injures capillary endothelial cells and increases cellular permeability [4] that are involved in the DNA damage of gastric mucosal epithelial cells [5]
Summary
The most common diseases include infectious diseases, gastric ulcer, cancer, diabetes, and liver and pancreas disease caused by alcohol consumption either partially or entirely [1]. Ethanol is absorbed through the intestinal wall and metabolized in the liver in different ways: oxidation by alcohol dehydrogenase (ADH), cytochrome P450 2E1. Alcohol metabolism with ADH enhances the generation of reduced forms of nicotinamide adenine dinucleotide (NADH), but production of CYP2E1 continues to produce free radical. Oxidative stress plays a crucial role in the pathogenesis of alcoholic tissue damage and increases lipid peroxidation, which injures capillary endothelial cells and increases cellular permeability [4] that are involved in the DNA damage of gastric mucosal epithelial cells [5]. The complete mechanism of alcohol-induced gastric mucosal damage has not been fully disclosed, evidence shows that oxidative stress and neutrophil infiltration are associated with the development of acute gastritis [6,7]
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