Protective effect of standardised fruit extract of Garcinia cowa Roxb. ex Choisy against ethanol induced gastric mucosal lesions in Wistar rats

Abstract

Background and aim The fruit of Garcinia is a rich and valuable source of bioactive compounds and is traditionally used for treating wounds and ulcers. The present study was carried out to investigate the protective effect of chromatographically standardized fruit extract of Garcinia cowa (GCE) on ethanol-induced gastric lesions in rats and its possible mechanisms. Methods The effect of GCE (200 and 400 mg/kg body weight) was evaluated by determining various gastric ulcer parameters like gastric wall mucus, non-protein sulfhydryls (NP-SH) content, microvascular permeability, endogenous antioxidant enzyme, and gastric histopathological study. Results and conclusions Oral administration of GCE at doses of 200 and 400 mg/kg exhibited significant ( p < .01) dose-dependent inhibition of ulcer index by 18.94–44.02%, respectively. Pre-treatment of rats with GCE (400 mg/kg) significantly restored the depleted gastric wall mucus level by 34.09% and NP-SH content by 33.35% induced by ethanol administration. In addition, GCE (400 mg/kg) showed a significant decrease in microvascular permeability of Evans Blue by 47.43%, rationalizing its protective effect. Furthermore, a significant increase in oxidative enzyme levels with reduction in malondialdehyde level and elevation of superoxide dismutase (SOD) activity was observed in the GCE treated group as compared to the ulcer control group. The histopathological assessment also confirmed the protective nature of GCE. HPTLC analysis showed the presence of 0.27%, 0.11% w/w gallic acid, and amentoflavone, respectively in GCE. The content of α-mangostin and xanthochymol in the G. cowa extract sample quantified by HPLC-PDA method was 0.72 and 8.46%, respectively. The results obtained indicate that the protective effect of GCE against gastric ulcers in rats through multiple actions confirmed by the reduction of oxidative stress and restoration of adhered gastric mucus, NP-SH content, and histological architecture. KEY MESSAGES Ethanol is the most typical ulcerogenic agent and has been shown to extend the risk of ulcer in humans. Natural products are promising alternative medication for the development of new drugs to regulate gastrointestinal diseases. Garcinia cowa protects the gastric mucosa through multiple actions that include restoration of adhered gastric mucus and inhibition of lipid peroxidation.

RNA-Seq Reveals Protective Mechanisms of Mongolian Medicine Molor-Dabos-4 on Acute Indomethacin-Induced Gastric Ulcers in Rats

“…In addition, the contents of piperine and piperidine were identified as 23.54% and 4.43% respectively, which were proved to be anti-inflammatory and antioxidant components in PLL and ginger [ 45 , 46 ]. Gupta et al showed that gallic acid had antiulcer effects through antioxidation, and the results of this study showed that the content of gallic acid in MD-4 was 12.02% [ 47 ]. The findings of this study thus support the above studies by suggesting that the compounds present in MD-4 could display protective effects mainly by modulating inflammatory and antioxidant mechanisms.…”

Repeated 28-Day Oral Toxicological Study and Gastroprotective Effects of Nigella sativa L. Oil (Shuhada) against Ethanol-Induced Gastric Mucosal Injury in Rats

“…Therefore, it can be assumed that N. sativa seed from Saudi Arabia have a high gastroprotective effect in the ethanol-induced gastric ulcer rat model. Several studies have shown that stimulated production of gastric wall mucus and reduced gastric acidity prevent ethanol-induced gastric ulcers [ 14 , 15 , 16 , 17 ]. It was hypothesized that BSO can effectively reduce the gastric ulcer area by stimulating the production of gastric wall mucus and suppressing gastric acidity, compared with the control pretreatment (distilled water).…”

Dendrobium officinale Flowers Flavonoids Enriched Extract Protects against Acute Ethanol-induced Gastric Ulcers via AMPK/PI3K Signaling Pathways

“…NP-SH plays an important role in tissue protection by scavenging prooxidants, endogenous NP-SH complex is a major component in mucosal protection against ethanol-induced stomach damage [60]. Assay results showed that ethanol significantly decreased gastric mucosal NP-SH level compared to the control group (P < 0.01).…”