Effect of various doses of palm vitamin E and tocopherol on aspirin‐ induced gastric lesions in rats

Abstract

Summary. This study examined the effects of vitamin E on the prevention of aspirin-induced gastric lesions. The study was divided into two phases. Phase 1 determined the effects of various doses of palm vitamin E on the factors affecting mucosal integrity. Thirty-two male rats of the Sprague-Dawley strain (200±250 g) were randomly divided into four groups. Group I was fed a normal diet (control), Groups II, III and IV were fed a diet supplemented with palm vitamin E in a dose of 60 mg/kg food, 100 mg/kg food and 150 mg/kg food, respectively. The rats were killed after 4 weeks of feeding for the determination of gastric malondialdehyde (MDA), acid and mucus content. There was a significant decrease in gastric MDA and gastric acid in all the palm vitamin E supplemented groups compared to control. However, these doses of palm vitamin E had no significant effect on gastric mucus. The phase 2 study determined the effect of multiple doses of palm vitamin E and tocopherol on the prevention of aspirin-induced gastric lesions. Fifty rats of the same weight and strain were randomized into seven groups. Group I was fed a normal diet; groups II to IV were fed with a palm vitamin E enriched diet in doses of 60 mg, 100 mg and 150 mg/kg food, respectively; groups V to VII were fed with a tocopherol-enriched diet in doses of 20 mg, 30 mg and 50 mg/kg food, respectively. After 4 weeks of feeding with the respective diets the rats were challenged with a single intra-gastric dose of 400 mg/kg body weight aspirin suspended in propylene glycol. The rats were killed 6 h post-aspirin exposure for the determination of gastric lesion index and gastric parameters as mentioned in the phase I study. The gastric lesions index was significantly lower in all the vitamin E groups compared to control. The lowest ulcer index was

Effects of Grape Seed Extract, Vitamin C, and Vitamin E on Ethanol- and Aspirin-Induced Ulcers

“…Although the decreases of MDA levels with GSE ( ≅ 83%) were greater than with VC ( ≅ 61%) or VE ( ≅ 77%), it should be noted that ethanol ulcer reduction with GSE was greater than MDA decreases, consistent with the fact that the protection of GSE against ethanol-induced ulcers depends not only on its scavenging properties, but on its ability for lowering increase MPO and consequent neutrophil infiltration [25, 46] as well. …”

Suppressive Effects of Natural and Synthetic Agents on Dextran Sulfate Sodium-induced Interleukin-1β Release from Murine Peritoneal Macrophages

“…Tel: +81-75-753-6281; Fax: +81-75-753-6284; E-mail: ohigashi@kais.kyoto-u.ac.jp Abbreviations: IL, interleukin; UC, ulcerative colitis; CD, Crohn's disease; IBD, inflammatory bowel disease; TNF, tumor necrosis factor; DSS, dextran sulfate sodium; pM, peritoneal macrophages; NAC, N-acetylcysteine; BHA, butylated hydroxyanisole; COX, cyclooxygenase; iNOS, inducible nitric oxide synthase; DMSO, dimethylsulfoxide; BITC, benzyl isothiocyanate; PPAR, peroxisome proliferator-activated receptor; NO, nitric oxide; IR, inhibitory rate; CV, cell viability; MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; EGCG, (À)-epigallocatechin gallate rutin and gallic acid (natural compounds, each at 100 M), were highly suppressive (IRs ¼ 72:8, 67.8 and 58.9%, and 79.3, 68.6 and 64.7%, respectively, P < 0:01 each). Our data may provide some insight into the molecular mechanisms by which -tocopherol 12) and rutin 13) suppress inflammation-related biological phenomena. The synthetic compounds, 1400W, meloxicam, bezafibrate and acetylsalicylic acid (at 100 M), and benzyl isothiocyanate (BITC), (À)-catechin and silymarin (natural compounds at 100 M) showed moderate inhibition (IRs ¼ 45:7, 38.4, 35.3 and 29.8%, and 53.9, 52.3 and 21.8%, respectively, P < 0:01 or P < 0:05).…”

Current approaches to prevent NSAID‐induced gastropathy – COX selectivity and beyond

“…Comedication with vitamin C abolished these effects, was able to scavenge free radicals, and significantly attenuated gastric damage [90]. In animal studies vitamin E protected against ASA‐induced gastric injury by inhibition of lipid peroxidation and accumulation of activated neutrophils [92, 93]. Both vitamins C and E seem to play a role in the preservation of gastric mucosal integrity; vitamin C is actively secreted into the gastric lumen of healthy subjects, and its concentrations are decreased in patients with gastroduodenal diseases such as peptic ulcer disease, gastric malignancy [94, 95], or H. pylori ‐associated gastritis [96].…”