Pure tocotrienol concentrate protected rat gastric mucosa from acute stress-induced injury by a non-antioxidant mechanism

Abstract

Stress has been implicated as a risk factor of various major health problems, such as stress-induced gastric mucosal injury. This study was performed to investigate the action of a pure preparation of tocotrienol (T3) concentrate, made up of 90% δ-tocotrienol and 10% γ-tocotrienol, on gastric injury of rats induced by water-immersion restraint stress (WIRS). Fourteen male Sprague-Dawley rats (200-250 g) were divided into two equal groups: a control group and a treated group. The treatment group received T3 concentrate at 60 mg/kg body weight daily for 28 days. The body weights of rats were recorded daily before the treatment was given. At the end of the treatment period, all rats were subjected to WIRS for 3.5 hours, following which the rats were euthanized. The stomachs were isolated and opened along the greater curvature for the examination of lesions and measurements of gastric malondialdehyde (MDA) and prostaglandin E 2 (PGE 2 ) contents. The mean gastric mucosal lesion index in the treated rats was significantly lower than that in the control rats. This suggests that the T3 concentrate has the ability to confer protection to the gastric mucosa against gastric injury induced by acute stress. No significant difference was observed for changes in body weight before and after the treatment. The gastric PGE 2 content in both groups was comparable. However, the gastric MDA content was significantly higher in the treated group compared to the control group, indicating that the T3 supplementation was not able to reduce the lipid peroxidation process. This study concludes that the T3 concentrate has the ability to protect the gastric mucosa from stress-induced injury by a non-antioxidant mechanism.

Preventive Effects of Tocotrienol on Stress-Induced Gastric Mucosal Lesions and Its Relation to Oxidative and Inflammatory Biomarkers

“…Research has shown the importance of maintaining a balance between the destructive and the protective capacity of the gastric mucosa to prevent formation of such mucosal injuries [ 2 , 4 ]. Supplementation with vitamin E such as tocopherol and tocotrienol have been shown to reduce the formation of stress-induced gastric lesions as reported in previous studies [ 24 , 25 ]. The findings observed in the study by Ibrahim et al showed a significant reduction in mean gastric lesions in rats supplemented with palm-vitamin E (which contains 70% tocotrienol) and α-tocopherol (60 mg/kg body weight for 28 days).…”

Effects of δ‐tocotrienol on ochratoxin A—induced nephrotoxicity in rats

“…After 1 week‐adaptation, these rats were randomly enrolled into four groups, were treated for 14 days by gavage, as follows: Control group ( n = 6:rats received 1 ml of corn oil containing 10% DMSO; Delta group ( n = 6); rats treated with Delta (60 mg/ kg of body weight) dissolved in DMSO and later scaled to the required volume with corn oil; OTA group ( n = 6): rats treated with OTA (0.5 mg/kg of body weight) dissolved in 10% DMSO and then scaled to required volume with corn oil; OTA plus Delta group ( n = 6): rats treated with Delta (60 mg /kg of body weight) plus OTA (0.5 mg/kg kg of body weight). The doses and times of Delta and OTA administration were chosen according to previous experiments (Ciarcia et al, ; Rodzian, Aziz Ibrahim, Nur Azlina, & Nafeeza, ). The rats were weighed at baseline (before receiving the first dose), five, 10, and at the end of the 14 days treatment.…”

Potential Role of Tocotrienols on Non-Communicable Diseases: A Review of Current Evidence

“…Stress reduced the level of PGE 2 in the stomach at least by half of its normal level, which was accompanied by formation of lesions [226][227][228]. Interestingly, Rodzian et al (2013) found that the supplementation annatto T3, which mainly contains δT3 isomer, suppressed gastric PGE 2 level [229]. On the other hand, palm pure T3 mixture was able to protect the gastric mucosa with the elevation of PGE 2 level, which was associated with an increased in cyclooxygenase-1 (COX-1) expression [221].…”