Effect of hydroalcoholic extract of Hibiscus rosa sinensis Linn. leaves in experimental colitis in rats

Objective: The present study was designed to evaluate the effect of hyperhomocysteinemia (Hhcy) induced by feeding rats high methionine diet on the colon wall. Colonic damages caused by Hhcy were compared with those induced by acetic -acid induced colitis.Methods: Sprague-Dawley rats (200-250g) were divided into four groups: group C (control), group M (received 1 g/kg methionine p. o. during 15 d), group A (colitis was induced by transrectal administration of acetic acid 4% on 8 th day) and group MA (received methionine and acetic acid). At the end of the study, plasma homocysteine, C-reactive protein (CRP) and leukocytes (WBC) count were evaluated, all rats were sacrificed and distal 8 cm of the colon was dissected. Colon was weighed for disease activity index (DAI) and injuries were assessed macroscopically and histologically.Results: High methionine diet induced significant (P<0.001) increase of homocysteine (hcy), CRP levels and WBC count compared to control. Acetic acid rats showed a significant decrease of WBC count. Mixed treatment caused a significant increase of hcy, CRP and a significant decrease of WBC count. Our results showed that Hhcy causes significant damages and immune cells infiltration in all layers of the colonic wall. Conclusion:The present investigation demonstrated that Hhcy increased the major inflammatory markers as CRP and leukocytes count and produced transmural colitis in rats. Effect of Hhcy is more toxic on the colonic wall than acetic acid indeed while acetic acid lesions are localized in mucosa and submucosa the lesions of hcy extend to the all layers (mucosa, submucosa and muscularis propria). Acetic acid induced colitis in hyperhomocysteinemic rats increased the severity of colitis.

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“…The acetic acid group showed a significant decrease of total leukocytes which is in agreement with Kandhare et al [12].…”

Section: Discussionsupporting

confidence: 91%

“…o.) [11]; (3) group A: acetic acid control rats (received 2 ml acetic acid 4% intrarectally on the 8th day) [12]; (4) group MA: received L-methionine 1g/kg/day, p. o. and acetic acid (4%) via intrarectal; The rat body weight and food intake was monitored daily for 15 d of the experiment.…”

Section: Experimental Designmentioning

confidence: 99%

Hyperhomocysteinemia Lead to Transmural Inflammation of Colon and Increase Severity of Disease in Acetic Acid-Induced Colitis in Rat

Souad

Naïmi

Cherifa

2017

Int J Pharm Pharm Sci

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“…72,73 It has been recognized that generation of oxidative stress subsequent to ischemia reperfusion injury was noticeably allied with mitochondrial DNA damage through exhaustion of thiols such as glutathione in isolated cells. 33,74 Moreover, it is renowned that apoptosis was triggered by involvement of proteases, nucleases, and phospholipases through rise in intra-mitochondrial pH 75 or from calcium released from mitochondria into the cytosol.…”

Section: +mentioning

confidence: 99%

Renoprotective effect of berberine via intonation on apoptosis and mitochondrial-dependent pathway in renal ischemia reperfusion-induced mutilation

2015

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Ischemic acute renal failure is a condition that extends subsequent to sudden and momentary fall in overall or regional blood flow to the kidney. The present investigation was deliberated to scrutinize the renoprotective potential of berberine in animal model of renal ischemia reperfusion (RIR) induced dent via assessment of various biochemical and molecular biomarkers. Male Wistar rats were anesthetized and the right kidney was removed through a small flank incision. Renal ischemia reperfusion was persuaded in uni-nephrectomized rats by occlusion of left renal artery for 45 min and reperfusion for 4 weeks. After 4 weeks of treatment of berberine (10, 20, and 40 mg/kg, p.o.), hemodynamic and left ventricular function were evaluated. Induction of ischemia reperfusion resulted callous mutilation in kidney which was confirmed by alterations in oxidative stress (SOD, GSH, and MDA), membrane bound enzymes, kidney function markers (serum creatinine and BUN), and mitochondrial dysfunction. Moreover, RIR injury exhibited incredible alterations in mRNA expression of KIM-1, NGAL, Caspase-3, Bax, Bcl-2, and TNF-a levels. Conversely treatment of berberine (20 and 40 mg/kg) significantly (p50.01 and p50.001) restored ischemia reperfusion induced marring via intonation of biochemical and molecular biomarkers. To sum up, berberine demonstrated compelling renoprotective effect in RIR injury via caspase-mitochondria-dependent pathway.

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“…Several studies concluded that polyunsaturated fatty acids are most vulnerable to free radical attacks and the initial products of lipid peroxidation are conjugated dienic hydroperoxide [43][44][45] . It involves the formation and propagation of lipid radicals, the uptake of oxygen and rearrangement of double bonds in unsaturated lipids which eventually results in destruction of membrane lipids [41][42][43][44][45][46] .…”

Section: Discussionmentioning

confidence: 99%

“…It involves the formation and propagation of lipid radicals, the uptake of oxygen and rearrangement of double bonds in unsaturated lipids which eventually results in destruction of membrane lipids [41][42][43][44][45][46] . Biological membranes are often rich in unsaturated fatty acids and bathed in oxygen-rich metal containing fluid 47,48 .…”

Section: Discussionmentioning

confidence: 99%

Antiulcer Potential of Morin in Acetic acid-Induced Gastric Ulcer via Modulation of Endogenous Biomarkers in Laboratory Animals

Bodhankar¹,

Sarkar²,

Sengupta³

et al. 2015

Pharmacologia

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Background: Peptic ulcer disease is a result of an imbalance between aggressive and defensive factors. Morin, a bioflavonoid exhibits many biological activities such as antioxidant and anti-inflammatory properties. Objective: The present study was conducted to unravel the therapeutic potential of morin in acetic acid-induced gastric ulcer. Materials and Methods: Gastric ulcer was induced in male Wistar rats (180-220 g) by applying glacial acetic acid (10 M, 100 μL) to serosa of the stomach. Morin (10, 30 and 100 mg kgG 1 , p.o.) was administered for 15 days after the induction of ulcer. After end of treatment gastric specimens were collected for biochemical and histological evaluation. Results: There was a significant (p<0.01 and p<0.05) reduction in the ulcer area and ulcer index by morin (30 and 100 mg kgG 1 ) treatment. It also significantly (p<0.01 and p<0.05) decreased the level of malondialdehyde (MDA) and increased levels of superoxide dismutase (SOD) as well as reduced glutathione (GSH). Histological aberration induced by acetic acid also reduced by morin administration. Conclusion: The present findings elucidate the antiulcer potential of morin in the acetic acid induced gastric ulcer by virtue of its antioxidant property.

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Effect of hydroalcoholic extract of Hibiscus rosa sinensis Linn. leaves in experimental colitis in rats

Cited by 99 publications

References 25 publications

Hyperhomocysteinemia Lead to Transmural Inflammation of Colon and Increase Severity of Disease in Acetic Acid-Induced Colitis in Rat

Hyperhomocysteinemia Lead to Transmural Inflammation of Colon and Increase Severity of Disease in Acetic Acid-Induced Colitis in Rat

Renoprotective effect of berberine via intonation on apoptosis and mitochondrial-dependent pathway in renal ischemia reperfusion-induced mutilation

Antiulcer Potential of Morin in Acetic acid-Induced Gastric Ulcer via Modulation of Endogenous Biomarkers in Laboratory Animals

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