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Articles by Amit D. Kandhare
Total Records ( 5 ) for Amit D. Kandhare
  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.
  Amit D. Kandhare , Mithun V.K. Patil and Subhash L. Bodhankar
  Background: Inflammatory Bowel Disease (IBD) is a chronic inflammatory, an idiopathic disorder of intestine with unknown etiology. Alstonia scholaris Linn., R.Br. (family Apocynaceae) shown to possesses potent antioxidant and anti-inflammatory activity. Objective: To evaluate the effect of an alkaloidal fraction of leaves of Alstonia scholaris (AFEAS) against acetic acid induced IBD in laboratory rats. Materials and Methods: Colitis was induced in male Wistar rats (180-220 g) by intrarectal administration of acetic acid (2 mL, 4% (v/v)). Rats were either treated orally with AFEAS (20, 40 and 80 mg kg–1) or distilled water (10 mg kg–1) or prednisolone (2 mg kg–1). Various biochemical, molecular and histological parameter were assessed. Results: Intrarectal administration of 4% acetic acid resulted in significant modulation (p<0.05) of serum alkaline phosphatase, lactate dehydrogenase, SOD, GSH, MDA and MPO content along with colonic NO, XO level and protein carbonyl content in the colonic tissue as well as in blood. The AFEAS (40 and 80 mg kg–1) administration significantly (p<0.05) ameliorated these acetic acid induced alteration in serum and colonic biochemical parameters. The decreased level of leptin and increased the level of pro-inflammatory cytokines (TNF-α and IL-1β) after acetic acid administration were significantly inhibited by AFEAS (40 and 80 mg kg–1) treatment. The AFEAS treatment reduced histological insult induced in the colon after intrarectal instillation of acetic acid. Conclusion: Treatment of AFEAS ameliorates acetic acid induced colitis by virtue of its anti-inflammatory and anti-oxidant potential via inhibition of production oxido-inflammatory mediator and pro-inflammatory cytokines.
  Anwesha Mukherjee , Amit D. Kandhare and Subhash L. Bodhankar
  Background: Clinically Gentamicin (GM) is commonly used aminoglycoside antibiotic for the treatment of life-threatening Gram-negative bacterial infections, but the nephrotoxic potential of drug limit its clinical interest. Chrysin a plant flavonoid possess potent antioxidant and anti-inflammatory activity. Objective: To investigate the potential of chrysin against GM-induced nephrotoxicity. Materials and Methods: Nephrotoxicity was induced in male Sprague-Dawley rats (220-250 g) by intraperitoneal administration of gentamicin (120 mg kg–1) for 7 consecutive days. Rats were either treated with chrysin (10, 20 and 40 mg kg–1, p.o.) or methylprednisolone (12.5 mg kg–1, i.p.) or vehicle distilled water (10 mg kg–1, p.o.) for the 7 days. Various biochemical, molecular and histological parameters were assessed in serum and kidney. Results: The GM-administration significantly increased (p<0.001) the serum creatinine and Blood Urea Nitrogen (BUN) as well as renal malonaldehyde (MDA), Nitric Oxide (NO) along with renal Kidney Injury Molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) mRNA expressions. In addition, GM also significantly decreased (p<0.001) the renal superoxide dismutase (SOD), reduced glutathione (GSH) and mitochondrial enzymes (NADH dehydrogenase and cytochrome c oxidase) activities. However, rats treated with chrysin (10, 20 and 40 mg kg–1, p.o.) failed to produce any significant inhibition in altered levels of antioxidant, inflammatory, apoptosis, AKI markers and mitochondrial depleted enzymes. Histopathological abbreviations were also did not ameliorates by chrysin treatment. Conclusion: Chrysin failed to produce any significant protection against gentamycin-induced renal toxicity.
  Amit D. Kandhare , Anwesha A. Mukherjee , Swanand D. Pasalkar , Sandesh A. Ghate and Subhash L. Bodhankara
  Background: Hyperbilirubinemia is a most leading cause of neonatal readmission condition and occurred due to rise in the level of unconjugated bilirubin in the blood. Phototherapy is widely used for the treatment of neonatal hyperbilirubinemia. Objective: To study the effect of edixeon S series power Light Emitting Diodes (LED) on obstructive jaundice induced hyperbilirubinemia in laboratory animals. Material and Methods: Hyperbilirubinemia was induced in male Wistar rats (180-220 g) via ligation of common bile duct. Rats were exposure to LED (low (0.06 W m–2) and high (1.0 W m–2) irradiation for 5 h for 3 days after recovery from surgery. Control rats were exposed to normal day light for 3 days. After 24 h of 3 days of exposure, blood was withdrawn under anaesthesia and they were sacrificed by cervical dislocation to collect the hepatic tissue. Various biochemical and histopathological parameters were evaluated in serum and hepatic tissue. Results: The LED irradiation (low and high) treatment significantly (p<0.01 and p<0.001) decreased serum albumin, aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphates (ALP), gamma-glutamyl transferase (GGT), total bilirubin and direct bilirubin levels as compared with control treated rat. Decreased level of hepatic superoxide dismutase (SOD) and glutathione peroxidase (GSH) were significantly (p<0.01 and p<0.001) increased by LED irradiation (low and high) treatment. It also significantly (p<0.01 and p<0.001) reduced the elevated level of malondialdehyde (MDA) and Nitric Oxide (NO) levels in hepatic tissue. Histological alternation induced in liver was also reduced by LED irradiation. Conclusion: The LED irradiation treatment showed inhibition in the elevated bilirubin levels via modulation of hepatic biomarkers as well as elevated oxidative stress. The use of edixeon S series power LED may be beneficial in terms of low cost of LED emitters and power requirements which can make this LED phototherapy a useful and possibly a preferred modality for the treatment of neonatal jaundice.
 
 
 
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