Anti-ulcer role of herbomineral siddha drug — Thamira parpam on experimentally induced gastric mucosal damage in rats

2010 ◽  
Vol 29 (3) ◽  
pp. 161-173 ◽  
Author(s):  
M. Vasanthkumar ◽  
RP Parameswari ◽  
V. Vijaya Kumar ◽  
MK Sangeetha ◽  
V. Gayathri ◽  
...  
Keyword(s):  
Thiobarbituric Acid ◽  
Mucosal Damage ◽  
Gastric Volume ◽  
Gastric Mucosal Damage ◽  
Thiobarbituric Acid Reactive Substances ◽  
Pylorus Ligation ◽  
Ulcerogenic Activity ◽  
Per Oral ◽  
Experimentally Induced

Anti-ulcerogenic activity of Thamira parpam (TP) was investigated in two ulcer models (aspirin + pylorus ligation and HCl-ethanol). Aspirin—pylorus ligation (Asp 200 mg/kg-7 days + PL-4 hours) and HCl-ethanol (150 mM HCl in 70% ethanol) induction in rat resulted in elevation of thiobarbituric acid reactive substances (TBARS) and depletion of antioxidants (superoxide dismutase [SOD], glutathione [GSH], glutathione peroxidase [GPx]) with high ulcer scores (p < .01). In Asp + PL model, TP treatment showed mild inhibition on ulcer scores, changes in pH, gastric volume, total and free acidity, and elevation of TBARS and depletion of antioxidants. Compared to the ulcer-untreated rats (HCl-ethanol), the herbomineral drug TP treatment (0.5, 1, 2 mg/kg, per oral [p.o.]) attenuated the elevation of TBARS, decrease of antioxidants and nitrite (p < .05). Histopathological examinations were correlated with the antioxidant profile. In conclusion, the prophylactic cytoprotective nature of the herbomineral drug in experimentally induced ulcers could be mediated by its free radical quenching property.

Role of Lipoxygenases and the Lipoxin A4/Annexin 1 Receptor in Ischemia-Reperfusion-Induced Gastric Mucosal Damage in Rats

Pharmacology ◽  
2009 ◽  
Vol 84 (5) ◽  
pp. 294-299 ◽  
Author(s):  
Brigitta M. Peskar ◽  
Karlheinz Ehrlich ◽  
Rufina Schuligoi ◽  
Bernhard A. Peskar
Keyword(s):  
Ischemia Reperfusion ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage ◽  
Lipoxin A4 ◽  
Annexin 1

scholarly journals Lens Lipid Peroxides and Glutathione Concentrations in Diabetic Cataract

1997 ◽  
Vol 34 (2) ◽  
pp. 190-192 ◽  
Author(s):  
D Özmen ◽  
I Mutaf ◽  
B Özmen ◽  
J Mentes ◽  
O Bayindir
Keyword(s):  
G Protein ◽  
Lipid Peroxide ◽  
Lipid Peroxides ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substances ◽  
Diabetic Cataract ◽  
Free Radical Damage ◽  
Significant Difference ◽  
Radical Damage

This study aims to explore the role of reactive oxygen radicals in the genesis of diabetic cataract. Lipid peroxide (LPO) concentrations in senile ( n = 30) and diabetic ( n = 14) cataractous lenses, were determined as thiobarbituric acid-reactive substances (TBARS) by a method modified from Satoh and Yagi, and reduced glutathione (GSH) concentrations were measured according to Beutler. Lens LPO levels (mean, SD; nmol TBARS/g protein) were significantly higher in diabetics (107·54, 18·12) than senile cataractous subjects (53·54, 15·48) ( P < 0·0001). Lens GSH levels (mean, SD; nmol/g protein) showed no significant difference between diabetics (4·29, 2·05) and senile cataractous subjects (4·68, 3·12). These results suggest that free radical damage is more effective in the genesis of diabetic cataract than in senile cataract.

scholarly journals Role of taurocholic acid in production of gastric mucosal damage after ingestion of aspirin.

BMJ ◽  
1975 ◽  
Vol 1 (5951) ◽  
pp. 183-185 ◽  
Author(s):  
K M Cochran ◽  
J F Mackenzie ◽  
R I Russell
Keyword(s):  
Mucosal Damage ◽  
Taurocholic Acid ◽  
Gastric Mucosal Damage

Role of vasoactive intestinal peptide (VIP) in pathogenesis of ethanol-induced gastric mucosal damage in rats

1993 ◽  
Vol 38 (7) ◽  
pp. 1210-1219 ◽  
Author(s):  
Fanny Karmeli ◽  
Rami Eliakim ◽  
Elimelech Okon ◽  
Daniel Rachmilewitz
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage

Role of nitric oxide in pathogenesis of gastric mucosal damage induced by compound in rats

1997 ◽  
Vol 91 (3-5) ◽  
pp. 131-138 ◽  
Author(s):  
T Yasuhiro ◽  
A Konaka ◽  
H Ukawa ◽  
S Kato ◽  
K Takeuchi
Keyword(s):  
Nitric Oxide ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage

Effects of sucralfate on gastric prostaglandin and leukotriene synthesis: relationship to protective actions

1988 ◽  
Vol 66 (5) ◽  
pp. 666-670 ◽  
Author(s):  
John L. Wallace ◽  
Gerald P. Morris ◽  
Paul L. Beck ◽  
Todd E. Williamson ◽  
Guy R. Gingras
Keyword(s):  
Ex Vivo ◽  
Protective Action ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage ◽  
Myeloperoxidase Activity ◽  
Protective Actions ◽  
Cyclooxygenase Activity ◽  
Chamber Model ◽  
Irritant Action

The mechanism of the protective actions of sucralfate against ethanol-induced gastric mucosal damage in the rat has been investigated. In particular, the role of prostaglandins as mediators of such protection was assessed. Oral administration of sucralfate at a dose causing a significant reduction of ethanol-induced gastric damage (500 mg/kg) did not significantly alter gastric 6-ketoprostaglandin F1α synthesis. Pretreatment with indomethacin at a dose that inhibited gastric cyclooxygenase activity by an average of 88% did not affect the protective actions of sucralfate. To further investigate the mechanism of action of sucralfate, an ex vivo gastric chamber model was used in which sucralfate could be applied to only one side of the mucosa. Sucralfate did not affect gastric prostaglandin synthesis, but did cause a significant increase in leukotriene C4 synthesis, a fall in transmucosal potential difference, and a significant decrease in gastric myeloperoxidase activity on the side exposed to sucralfate. These observations suggest that sucralfate has an irritant action on the mucosa. The release of mediators in response to such irritation may play an important role in the protective action of sucralfate. The present study supports the hypothesis that prostaglandins do not mediate the protection afforded by exposure to sucralfate.

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