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Research Article

Anti-inflammatory action of Tamarind seeds reduces hyperglycemic excursion by repressing pancreatic β-cell damage and normalizing SREBP-1c concentration

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Pages 350-360 | Received 26 Jun 2012, Accepted 07 Sep 2012, Published online: 15 Nov 2012
 

Abstract

Context: Tamarindus indica L. (Leguminosae) is widely used as a traditional medicine for the management of diabetes mellitus (DM) in India, in addition to its anti-inflammatory activity. The present study has been designed to understand the correlation involved between antidiabetic and anti-inflammatory action of aqueous seed extract of T. indica (TSE) in diabetic rats.

Objective: In view of the fact that fatty acid synthesis and insulin release from islets of pancreas are regulated by sterol regulatory element-binding proteins (SREBP-1c) and cytosolic calcium, respectively, the objectives of present study were to determine the influence of TSE on SREBP-1c mRNA and to investigate the intracellular islets calcium [Ca2+]I involvement and β-cell mass preservation in insulin secretagogue action of TSE.

Materials and methods: The effect of 4 weeks oral treatment (120 and 240 mg/kg) of high-performance liquid chromatography (HPLC) standardized TSE was studied in streptozotocin (STZ)-induced diabetic male Wistar rats. Reverse transcription-PCR (RT-PCR) and a spectrofluorometer were used for mRNA concentration and islets [Ca2+]I determination, respectively. The TUNEL assay was followed to study the pancreatic apoptosis.

Results: TSE (120 and 240 mg/kg) showed positive correlation with [Ca2+]I and insulin release. The anti-inflammatory action of TSE was significant on nitric oxide (NO) and tumor necrosis factor-α (TNF-α) in addition to a favorable effect on β-cell neogenesis and improved mRNA concentration of SREBP-1c.

Discussion and conclusion: The results suggest that anti-inflammatory action of Tamarind seeds on β-cell cells of islets and cytokines contribute toward its antidiabetic activity by way of complex mechanisms of [Ca2+]I handling and through SREBP-1c gene in liver.

Acknowledgments

The author acknowledges Panacea Biotech and Ranbaxy, India for providing glimiperide and metformin, respectively.

Declaration of interest

The study was supported by Government of NCT Delhi [MH-2203-O.E.1.1(1)(1)(1)(4)], India. The authors report no declaration of interest.

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