The ameliorative effects of cinnamon oil against ethanol-induced gastric ulcer in rats by regulating oxidative stress and promoting angiogenesis.

Cinnamon is one of the herbal resources belonging to the Lauraceae family, is commonly used in traditional medicine and as a flavoring agent. It has antioxidant and anti-inflammatory activities. Therefore, the present study was performed to evaluate the gastroprotective effect of cinnamon on ethanol-induced gastric ulcer in comparison to omeprazole. In Wistar rats, gastric ulcers were induced using one oral dose of 70% ethanol (5 ml/kg b. w.) Cinnamon oil at doses of 2.5 ml/kg body weight and omeprazole (a reference drug) at a dose of 20 mg/kg body weight were orally administrated daily for 7 days before ulcer induction. 1 h after ethanol administration blood samples were collected and then the stomachs of sacrificed rats were subjected to biochemical, macroscopic and histological, and immunohistochemical studies. Oral administration of cinnamon oil significantly attenuated gastric ulcer as revealed by a significant increase in the gastric levels of enzymatic and non-enzymatic antioxidants namely CAT, SOD, GSH-Px, and GSH with a concomitant reduction in MDA level compared with those in the ethanol group. Pre-treatment of cinnamon oil markedly improved the level of TNF-α and PGE content. Furthermore, cinnamon oil pre-treatment significantly increased the immunoreactivity of VEGF while decreasing the immunoreactivity of COX-II. These results were further supported by histopathological findings which revealed the curing effect of cinnamon oil on the microscopic changes induced by ethanol toxicity. Cinnamon oil showed a potential gastroprotective effect on ethanol-induced gastric ulcer comparable to the gastroprotective effect of omeprazole, and its effect may be mediated through suppression of oxidative stress and gastric inflammation and promotion of angiogenesis.

Effect of gervital in attenuating hepatotoxicity caused by methotrexate or azathioprine in adult albino rats.

Methotrexate (MTX) and azathioprine (AZA) are chemotherapeutic, antimetabolic, and immunosuppressive agents with substantial risks such as oxidative lesions to the liver. This study examined the effect of grape seed extract (GSE; gervital) in attenuating hepatotoxicity caused by MTX or AZA treatment. Rats were divided into six groups (six rats per group): Group I, normal control group; Group II, GSE (150 mg/kg/day); Group III, MTX (8 mg/kg/week); Group IV, AZA (15 mg/kg/day); Group V, GSE (150 mg/kg/day) + MTX (8 mg/kg/week); and Group VI, GSE (150 mg/kg/day) + AZA (15 mg/kg/day). After 35-day experimental period, all rats were sacrificed and blood was collected for biochemical study and hemoglobin (Hb) assessment. The liver was weighed and triaged for histological, ultrastructural, and biochemical studies. MTX and AZA treatment decreased Hb levels, increased relative liver weight, increased the activity of glutamate pyruvate transaminase (ALT) and glutamate oxaloacetate transaminase (AST) aminotransferase (ALT) and aspartate aminotransferase (AST) values, and displayed histopathological and ultrastructural alterations. These changes included the disorganization of hepatocytes, pyknosis, karyolysis of some nuclei, and mononuclear leukocytic infiltration. The liver with significant oxidative stress (OS) showed decreased reduced glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) and increased malondialdehyde (MDA) levels. In contrast, GSE administration ameliorated ALT, AST, and all histopathological and ultrastructural changes. GSE treatment also reduced MDA levels but increased the antioxidant parameters. In conclusion, it was concluded that GSE supplementation could be considered as a promising antioxidant in reducing OS, histopathological and ultrastructural alterations induced by MTX and AZA.