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Articles by Antara Sengupta
Total Records ( 2 ) for Antara Sengupta
  Sandipan Sarkar , Antara Sengupta , Answesha Mukhrjee , Anamika Guru , Anagha Patil , Amit D. Kandhare and Subhash L. Bodhankar
  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 kg-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 kg-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.
  Amit D. Kandhare , Anagha Patil , Anamika Guru , Anwesha Mukhrjee , Sandipan Sarkar , Antara Sengupta , Hari Mohan Parmar , Amol P. Muthal , Pralhad Wangikar and Subhash L. Bodhankar
  Background: Inflammatory Bowel Disease (IBD) is a chronic disease of unknown etiology, which is characterized by chronic and spontaneously relapsing inflammation. Objective: To evaluate the effect of ferulic acid on acetic acid-induced IBD in rats. Materials and Methods: Ulcerative colitis was induced in male Wistar rats (180-220 g) by intrarectal instillation of 2 mL of 4% (v/v) acetic acid solution. Rats were treated orally with either ferulic acid (10, 20 and 40 mg kg–1, p.o.), prednisolone (2 mg kg–1) or distilled water (10 mg kg–1). Various biochemical, molecular and histological parameters were evaluated. Results: Intrarectal administration of 4% acetic acid resulted in significant alteration (p<0.05) in ulcer area, serum alkaline phosphatase, serum lactate dehydrogenase and colonic superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA) and myeloperoxidase (MPO) content. Administration of ferulic acid (20 and 40 mg kg–1) significantly (p<0.05) ameliorated these acetic acid-induced alterations. There was a significant (p<0.05) down-regulation in colonic HO-1 mRNA expression, which was significantly up-regulated (p<0.05) by ferulic acid (20 and 40 mg kg–1). The decreased colonic Nfr2 level after acetic acid instillation was increased by ferulic acid (20 and 40 mg kg–1) treatment, which was revealed by immunohistochemical analysis. Histological aberration induced after acetic acid instillation was inhibited by ferulic acid. Conclusion: The findings of the present investigation showed that ferulic acid has an anti-inflammatory and anti-oxidant potential to inhibit acetic acid-induced colitis via upregulation in the HO-1 and Nrf-2 expressions.
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