Protective effects of aqueous garlic extract in reducing water avoidance stress-induced degeneration of the stomach, ileum, and liver: morphological and biochemical study.

We investigated the effect of aqueous garlic extract (AGE) on water avoidance stress (WAS)-induced degeneration of the gastric and ileal mucosa and liver parenchyma. Wistar albino rats were exposed to WAS (WAS group) for 5 days. After exposure of the animals to WAS, a 1 ml/kg aqueous garlic extract (AGE) was injected i.p. (WAS+AGE group). The stomach, ileum, and liver samples were investigated under light microscope for general morphology. Topography of gastric and ileal mucosa was investigated by scanning electron microscopy, and hepatocyte ultastructure by transmission electron micsroscopy. Malondialdehyde (MDA) and glutathione (GSH) levels of all tissues were also determined. In the WAS group, the epithelium of the stomach showed ulceration in some areas, dilatations of the gastric glands, and degeneration of gastric glandular cells. Severe vascular congestion and degeneration of ileal epithelium were observed. Prominent vascular congestion and dilated sinusoids, activated Kupffer cells with prominent morphology, dilated granular endoplasmic reticulum membranes, and focal picnotic nuclei were observed in liver parenchyma. AGE treatment reduced the degeneration of the gastric and ileal mucosa and liver parenchyma. Increased MDA levels and decreased GSH levels in the WAS group were reversed to control values after AGE treatment. Based on these results, AGE treatment significantly prevented WAS-induced degeneration in both morphology and biochemistry of gastrointestinal mucosa and liver parenchyma due to its potent free radical scavenging and antioxidant properties.

Taurine ameliorates stress-induced degeneration of the urinary bladder.

We studied the potential effects of taurine, a free radical scavenger, on chronic water avoidance stress (WAS)-induced degeneration of the mucosa of the urinary bladder in experimental rats. Wistar albino rats were exposed to WAS for 2h/day, for 5 days (WAS group). Before exposing them to WAS, taurine (50mg/kg) (WAS+taurine group) was injected intraperitonally into the animals. Samples of urinary bladder were then investigated by light and scanning electron microscopy. Lipid peroxidation and gluthathione levels were also measured in the urinary bladder. In the WAS-only group, inflammatory cell infiltration, increased number of mast cells in the mucosa and ulcerated areas were observed. In the WAS+taurine group, relatively normal urothelial topography with microvilli, moderate inflammatory cell infiltration and decreased numbers of mast cells in the mucosa were observed. The increased lipid peroxidation and decreased glutathione levels in WAS rats were reversed by taurine treatment. We conclude that taurine protects against WAS-induced oxidant urinary bladder injury, and thus may be a possible therapeutic agent against interstitial cystitis, the symptoms of which are aggravated by stress conditions.

An aqueous garlic extract alleviates water avoidance stress-induced degeneration of the urinary bladder.

OBJECTIVE: To investigate the role of aqueous garlic extract (AGE) on the water-avoidance stress (WAS)-induced degeneration of the urinary bladder in a rat model. MATERIALS AND METHODS: Wistar albino rats were exposed to WAS for 2 h/day for 5 days (WAS group), after which, AGE (1 mL/kg) was injected intraperitoneally into the rats (WAS + AGE group). Urinary bladder samples were investigated with both light and scanning electron microscopy, and lipid peroxidation and glutathione levels were also measured in the samples. RESULTS: In the WAS group there was inflammatory cell infiltration, more mast cells and ulcerated areas in the mucosa. In the WAS + AGE group there was relatively normal urothelial alignment, moderate inflammatory cell infiltration and fewer mast cells in the mucosa. The increased lipid peroxidation and decreased glutathione levels in WAS rats were reversed by AGE treatment. CONCLUSIONS: These results show that AGE has a protective effect on WAS-induced degenerative changes in the urinary bladder.

Taurine ameliorates water avoidance stress-induced degenerations of gastrointestinal tract and liver.

We investigated the role of taurine, is a potent free radical scavenger, on water avoidance stress (WAS)-induced degeneration of the gastric, ileal, and colonic mucosa and liver parenchyma. Wistar albino rats were exposed to chronic WAS (WAS group) 2 hr daily for 5 days. After exposing animals to chronic WAS (WAS + taurine group), 50 mg/kg taurine was injected IP for 3 days. Control animals received vehicle solution only. The stomach, ileum, colon, and liver samples were investigated under light microscope for histopathologic changes. To demonstrate the topography of the luminal mucosa of the stomach, ileum, and colon, scanning electron microscope was used and for hepatocyte ultastructure transmission electron microscope was used. Malondialdehyde (MDA, a biomarker of oxidative damage) and glutathione (GSH, a biomarker of protective oxidative injury) levels were also determined in all tissues. In the WAS group, the stomach epithelium showed ulceration in some areas, dilatations of the gastric glands, and degeneration of gastric glandular cells; prominent congestion of the capillaries was apparent. In the WAS group, severe vascular congestion was observed along with degeneration of ileal and colonic epithelium. Prominent vascular congestion and dilated sinusoids, activated Kupffer cells, dilated granular endoplasmic reticulum membranes, and focal pyknotic nuclei were observed in liver parenchyma. MDA levels (stomach, P < 0.01; ileum, colon, and liver P < 0.05) were increased and GSH levels (P < 0.01) were decreased in all tissues in the WAS group compared with the control group. The morphology of gastric, ileal, and colonic mucosa and liver parenchyma in the WAS + taurine group (stomach and ileum, P < 0.05; colon and liver, P < 0.01) showed a significant amelioration when compared to the WAS group. Increased MDA and decreased GSH levels in the WAS group were ameliorated with taurine treatment. Based on the results, taurine supplementation effectively attenuates the oxidative damage of gastrointestinal mucosa and liver because of WAS induction possibly by its antioxidant effects.

Protective effects of taurine on protamine sulfate induced bladder damage.

The present study was designed to investigate the putative protective effects of taurine on protamine sulfate (PS) induced bladder injury. Wistar albino female rats were catheterized and intravesically infused with phosphate buffered solution (control group) or PS (PS group) dissolved in phosphate buffered solution. In the PS + taurine (PS+Tau) group, after the PS instillation, taurine (50 mg/kg) was injected intraperitoneally for 3 days. Histopathological changes were investigated by light and scanning electron microscopy. Tissue samples were also obtained to determine bladder malondialdehyde (MDA) (a biomarker of oxidative damage) and glutathione (GSH) (a biomarker of protective oxidative injury) levels. In the PS group ulcerated areas, an irregular mucus layer, inflammatory cell infiltration, and increased number of mast cells were observed. In the PS+Tau group, a relatively normal urothelial topography, glycosaminoglycan layer, and decreased number of mucosal mast cells and inflammatory cells were observed. Increased MDA levels as a result of PS induction lead us to propose that free radicals may have a critical role in this injury. The significant decrease in MDA and increase in GSH levels in the PS+Tau group compared to PS group was in accordance with morphological findings. Based on the results, taurine treatment significantly prevented PS induced degenerative morphological and biochemical changes of urinary bladder mucosa.

Aqueous garlic extract inhibits protamine sulfate-induced bladder damage.

This morphological and biochemical study aims to investigate the antioxidant effects of chronic administration of aqueous garlic extract (AGE) on protamine sulfate (PS)-induced bladder injury. Wistar albino female rats were catheterized and intravesically infused with phosphate-buffered solution (control group) or PS (PS group) dissolved in phosphate-buffered solution. In the PS + AGE group after the PS instillation, AGE (1 ml/kg, i.p., corresponding to 250 mg/kg) was injected intraperitoneally for 3 days. Bladder morphology was investigated by light and scanning electron microscopy. Tissue samples were also obtained to determine bladder malondialdehyde (MDA) and glutathione levels. In the PS group, ulcerated areas, an irregular mucus layer, inflammatory cell infiltration and an increased number of mast cells were observed. In the PS + AGE group a relatively normal urothelial topography, glycosaminoglycan layer and a decreased number of mucosal mast cells and inflammatory cells were observed. Increased MDA levels as a result of PS induction led us to propose that free radicals may have a critical role in this injury. The significant decrease in MDA and increase in glutathione levels in the PS + AGE group was in accordance with morphological findings. Based on the results, AGE treatment significantly prevented PS-induced degenerative morphological and biochemical changes of urinary bladder mucosa.