The Biological Activity of Propolis Against Gastric Ulcers

Gastric ulcer is a clinically common digestive system disorder with a high epidemiological incidence. Its pathogenesis is complex and diverse. Current academic consensus indicates that Helicobacter pylori infection, the use of non-steroidal anti-inflammatory drugs (NSAIDs), and exogenous damaging agents such as ethanol can disrupt the gastric mucosal barrier function. This leads to autodigestion of the gastric wall by gastric acid and pepsin, ultimately inducing the formation of peptic ulcers (Hu Fulian, 2005).

In recent years, substantial experimental research has confirmed that propolis and its extracts show significant protective and therapeutic potential against gastric ulcers induced by various pathogenic factors. Kim Ha-Gyu et al. (1996) systematically evaluated the anti-ulcer effects of an ethanol extract of propolis (EEP) using five experimental ulcer models, including pylorus-ligation, stress-induced, and ethanol-induced types. The results demonstrated that EEP not only effectively inhibited pepsin activity and reduced gastric acid secretion in the pylorus-ligation model but also promoted the healing process of acetic acid-induced ulcers. Furthermore, it significantly reduced the lesion area in other ulcer types, indicating broad-spectrum anti-ulcer properties of propolis extract.

Further research by Kim Chun-Ok et al. (1996), who separated propolis components via solvent extraction, found that its petroleum ether extract exhibited significant antagonistic effects against acetic acid-induced and stress-induced ulcers. The mechanism involved reducing free gastric acid concentration, increasing prostaglandin E2 (PGE2) levels, and enhancing gastric wall mucus secretion. In contrast, the n-butanol extract did not show significant anti-ulcer activity in these models but could still inhibit pepsin activity and promote mucus synthesis. It was thus inferred that the main active anti-ulcer components of propolis are concentrated in the petroleum ether-soluble fraction.

In international studies, de Barros et al. (2007) systematically investigated the protective effects of Brazilian green propolis against various experimental gastric ulcers, including ethanol-induced and indomethacin-induced types. The study indicated that pre-treatment with EEP at doses of 50, 250, and 500 mg/kg significantly reduced the ulcer index, total lesion area, and the ratio of lesion area to total stomach area in ethanol-induced ulcers. For indomethacin-induced and stress-induced ulcers, effective doses were 500 mg/kg and 250 mg/kg, respectively. In the pylorus-ligation model, higher doses (250 and 500 mg/kg) of green propolis exhibited clear antisecretory activity, manifested by reductions in gastric juice volume, total acidity, and pH. Subsequent compositional analysis suggested that the anti-ulcer effect of Brazilian green propolis is closely related to its phenolic acid components, such as caffeic acid, ferulic acid, p-coumaric acid, and cinnamic acid (de Barros, 2008).

Notably, Helicobacter pylori infection is closely associated with the occurrence and recurrence of gastric ulcers, and inhibiting this bacterium has become an important strategy in treatment. Research by Chen Lian (2009) showed that EEP inhibited the growth of H. pylori in a concentration-dependent manner, whereas the inhibitory effect of a water extract of propolis (WEP) was weaker. On the other hand, EI-Ghazaly et al. (2011) explored the effects of WEP on indomethacin-induced gastric ulcers under both irradiated and non-irradiated conditions. They found that oral pre-treatment with WEP effectively alleviated ulcer severity regardless of irradiation status. The mechanism involved inhibiting gastric acid secretion and digestive activity, promoting mucin and PGE2 synthesis, while significantly reducing levels of inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β), as well as inhibiting lipid peroxidation and malondialdehyde (MDA) generation. This confirms the multi-target role of propolis in gastric mucosal protection.

In summary, existing research fully demonstrates that propolis and its active components exhibit favorable preventive and therapeutic effects in various experimental gastric ulcer models through multiple mechanisms. These include regulating gastric acid secretion, inhibiting pepsin activity, enhancing mucosal defense capacity, and exerting anti-inflammatory and antioxidant actions. These findings provide a solid experimental pharmacological basis for the potential application of propolis as an adjunct in the clinical treatment of gastric ulcers. Future research should further focus on the isolation and identification of its specific active components, in-depth analysis of its action pathways, and systematic evaluation of its preclinical and clinical translation.

Reference:

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