Effect of lysozyme chloride on betel quid chewing aggravated gastric oxidative stress and hemorrhagic ulcer in diabetic rats

Chen-Road Hung, Chen-Road Hung

Abstract

Aim: To evaluate the protective effect of lysozyme chloride on betel quid chewing (BQC) aggravated gastric oxidative stress and hemorrhagic ulcer in rats with diabetes mellitus (DM).

Methods: Male Wistar rats were challenged intravenously with streptozotocin (65 mg/kg) to induce DM. Rats were fed with regular pellet food or BQC-containing diets. After 90 d, rats were deprived of food for 24 h. Rat stomachs were irrigated for 3 h with normal saline or simulated gastric juice. Rats were killed and gastric specimens were harvested.

Results: An enhancement of various gastric ulcerogenic parameters, including acid back-diffusion, mucosal lipid peroxide generation, as well as decreased glutathione levels and mucus content, were observed in DM rats. After feeding DM rats with BQC, an exacerbation of these ulcero-genic parameters was achieved. Gastric juice caused a further aggravation of these ulcerogenic parameters. Daily intragastric lysozyme chloride dose-dependently inhibited exacerbation of various ulcerogenic parameters in those BQC-fed DM rats.

Conclusion: (1) Gastric juice could aggravate both DM and BQC-fed DM rat hemorrhagic ulcer; (2) BQC exacerbated gastric hemorrhagic ulcer in DM rats via enhancing oxidative stress and reducing defensive factors; (3) lysozyme chloride effectively protected BQC aggravated gastric damage in DM rats.

Figures

Figure 1
Figure 1
Histological studies of gastric mucosa exposed for 3 h gastric juice in normal, DM, and BQC-fed DM rats. Note that in normal rat stomachs irrigated with gastric juice (A), gastric mucosal cells look intact. However, gastric juice- irrigated DM rat mucosa (B), a disruption of gastric epithelial layer is observed. When stomachs of BQC-fed DM rats are irrigated with gastric juice (C), a complete disruption of the upper mucosal cells and lamina propria is obtained. The injured cells are characterized by karyorrhexis and dense homogenous acidophilic cytoplasm. In most cases, gastric edema also is observed (×150).
Figure 2
Figure 2
Histological scores of gastric mucosa in normal, DM, and BQC-fed DM rats. Rats were fed with normal diet or BQC diet for 90 d. Diabetes was induced by intravenous streptozotocin. Rat stomachs were irrigated for 3 h with normal saline (□) or gastric juice (■). Values are mean SE, n = 6-8. Bars labeled with different letters are significantly different at P < 0.05 based on Tukey statistic method.

Source: PubMed

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