Palm vitamin E and the healing of ethanol-induced gastric lesions

Ismail, Nafeeza Mohd

doi:10.1046/j.1440-6047.1999.00097.x

Cited by 11 publications

(5 citation statements)

References 10 publications

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“…Gastric ulcers induced by ethanol exposure in rats were significantly reduced with the supplementation of PVE at 150 mg/kg in food for 3 weeks [249,250]. The ulcers healing was also accelerated when PVE (150 mg/kg food) was given post-ulcer induction with ethanol [249].…”

Section: Effects Of Tocotrienol On Peptic Ulcersmentioning

confidence: 99%

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

et al. 2020

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Tocotrienol (T3) is a subfamily of vitamin E known for its wide array of medicinal properties. This review aimed to summarize the health benefits of T3, particularly in prevention or treatment of non-communicable diseases (NCDs), including cardiovascular, musculoskeletal, metabolic, gastric, and skin disorders, as well as cancers. Studies showed that T3 could prevent various NCDs, by suppressing 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) in the mevalonate pathway, inflammatory response, oxidative stress, and alternating hormones. The efficacy of T3 in preventing/treating these NCDs is similar or greater compared to tocopherol (TF). TF may lower the efficacy of T3 because the efficacy of the combination of TF and T3 was lower than T3 alone in some studies. Data investigating the effects of T3 on osteoporosis, arthritis, and peptic ulcers in human are limited. The positive outcomes of T3 treatment obtained from the preclinical studies warrant further validation from clinical trials.Nutrients 2020, 12, 259 2 of 84 Nutrients 2020, 12, 259 4 of 84 the order δ > γ > β > α [45]. Using HepG2 cells, γT3 was shown to stimulate apolipoprotein B (Apo-B) degradation by decreasing its translocation into the endoplasmic reticulum (ER) lumen. This action eventually caused a reduction in the number of Apo-B in lipoprotein particles [46]. Other reports showed that γT3 and δT3 had the potential to reduce the hepatic TG synthesis and very-low-density lipoprotein (VLDL) secretion by suppressing expression of genes involved in lipid homeostasis, particularly the TG, cholesterol, and VLDL biosynthesis. Moreover, δT3 also promoted the efflux of LDL through LDL receptor expression [47]. A summary of the literature on effect of T3 supplementation on lipid profile of hypercholesterolemic model in vitro is shown in Table 1.Animal models of dyslipidemia have been used to investigate the effects of T3 on lipid profile. Several animals have been tested, including chicken, swine and rodents (rats, hamsters, guinea pigs). In chickens fed with a varying level of αTF and γT3, Qureshi et al. (1996) showed that αTF enhanced the inhibition of HMGCR by γT3. They further stipulated that the vitamin E mixture should contain 15-20% of αTF and approximately 60% of γT3 or δT3 for optimal anti-cholesterol effects [48]. In the subsequent study, demonstrated that combination of 50 ppm T3-rich fraction (TRF) and 50 ppm lovastatin was more effective in suppressing HMGCR activity compared to lovastatin alone in chickens. The combination also reduced serum TC and LDL-C, TG, Apo-B, thromboxane B 2 , and platelet factor 4 in contrast to individual treatment [49]. Using chicken supplemented with 50 ppm of δT3, Qureshi et al. (2011) further revealed that δT3 reduced TC and LDL-C besides suppressing the lipid elevating effects of dexamethasone and potentiated the TG-lowering effect of riboflavin [50]. Using genetically hypercholesterolemic swine, Qureshi et al. (1991) demonstrated the significant effect of TRF in lowering serum TC, LDL-C, Apo-B, thrombo...

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Section: Effects Of Tocotrienol On Peptic Ulcersmentioning

confidence: 99%

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

et al. 2020

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“…[16] but which has since been modified by Ismail et al . [17]. The modified scale used was as follows: 5 = continuous lesions that occupied almost the entire length of the gastric fold, 4 = lesions which occupied almost 80% of the entire fold, 3 = presence of multiple lesions that measured 1-4 mm in length on 80% of the folds, 2 = presence of at least two lesions approximately 2 mm in length, 1 = presence of a single lesion with or without generalized erythema, 0.5 = presence of dot haemorrhages; and 0 = no visible damage.…”

Section: Methodsmentioning

confidence: 99%

Experimental research Effects of captopril on factors affecting gastric mucosal integrity in aspirin-induced gastric lesions in Sprague-Dawley rats

Ibrahim¹,

Hashim²,

Jaarin³

2013

aoms

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IntroductionCaptopril is an angiotensin-converting enzyme inhibitor, which is used as an antihypertensive agent and has shown antioxidant properties. This study aims at determining the effects of captopril on factors affecting gastric mucosal integrity in aspirin-induced gastric lesions.Material and methodsEighteen male Sprague-Dawley (200-250 g) rats that were given aspirin (40 mg/100 g body weight) were divided into three groups: the control, captopril (1 mg/100 g body weight daily) and ranitidine (2.5 mg/100 g body weight twice daily) groups. Ranitidine and captopril were given orally for 28 days. Rats in all groups were sacrificed and the parameters measured.ResultsCaptopril reduced gastric acidity, and increased gastric glutathione (GSH) and prostaglandin E2 (PGE2) significantly in comparison to the control group. Captopril also reduced malondialdehyde (MDA) and gastric lesions insignificantly compared to the control group. Ranitidine healed the lesions significantly compared to the control group. There was no difference between ranitidine and captopril on the severity of lesions, gastric acidity, MDA and GSH. Captopril increased PGE2 compared to ranitidine (p < 0.05).ConclusionsCaptopril has desirable effects on the factors affecting gastric mucosal integrity (acidity, PGE2 and GSH) and is comparable to ranitidine in ulcer healing.

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“…The macroscopic assessment of aspirin-induced gastric lesions was performed by an independent examiner who was blinded to the supplementation that the rats had received. The assessment of lesions was made according to a semi-quantitative scale described earlier by Berry et al [16] but which has since been modified by Ismail et al [17]. The modified scale used was as follows: 5 = continuous lesions that occupied almost the entire length of the gastric fold, 4 = lesions which occupied almost 80% of the entire fold, 3 = presence of multiple lesions that measured 1-4 mm in length on 80% of the folds, 2 = presence of at least two lesions approximately 2 mm in length, 1 = presence of a single lesion with or without generalized erythema, 0.5 = presence of dot haemorrhages; and 0 = no visible damage.…”

Section: Methodsmentioning

confidence: 99%

Effects of captopril on factors affecting gastric mucosal integrity in aspirin‐induced gastric lesions in Sprague‐Dawley rats

2012

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I In nt tr ro od du uc ct ti io on n: : Captopril is an angiotensin-converting enzyme inhibitor, which is used as an antihypertensive agent and has shown antioxidant properties. This study aims at determining the effects of captopril on factors affecting gastric mucosal integrity in aspirin-induced gastric lesions. M Ma at te er ri ia al l a an nd d m me et th ho od ds s: : Eighteen male Sprague-Dawley (200-250 g) rats that were given aspirin (40 mg/100 g body weight) were divided into three groups: the control, captopril (1 mg/100 g body weight daily) and ranitidine (2.5 mg/100 g body weight twice daily) groups. Ranitidine and captopril were given orally for 28 days. Rats in all groups were sacrificed and the parameters measured. R Re es su ul lt ts s: : Captopril reduced gastric acidity, and increased gastric glutathione (GSH) and prostaglandin E 2 (PGE 2 ) significantly in comparison to the control group. Captopril also reduced malondialdehyde (MDA) and gastric lesions insignificantly compared to the control group. Ranitidine healed the lesions significantly compared to the control group. There was no difference between ranitidine and captopril on the severity of lesions, gastric acidity, MDA and GSH. Captopril increased PGE 2 compared to ranitidine (p < 0.05). C Co on nc cl lu us si io on ns s: : Captopril has desirable effects on the factors affecting gastric mucosal integrity (acidity, PGE 2 and GSH) and is comparable to ranitidine in ulcer healing. K Ke ey y w wo or rd ds s: : captopril, ranitidine, aspirin, gastric lesions.C Co or rr re es sp po on nd di in ng g a au ut th ho or r: :

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Palm vitamin E and the healing of ethanol-induced gastric lesions

Cited by 11 publications

References 10 publications

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

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

Experimental research Effects of captopril on factors affecting gastric mucosal integrity in aspirin-induced gastric lesions in Sprague-Dawley rats

Effects of captopril on factors affecting gastric mucosal integrity in aspirin‐induced gastric lesions in Sprague‐Dawley rats

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