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Cellmed Orthocellular Medicine and Pharmaceutical Association (셀메드 세포교정의약학회)
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Potential mechanism of anti-diabetic activity of Picrorhiza kurroa

  • Husain, Gulam Mohammed (Neuropharmacology Research Laboratory, Department of Pharmaceutics, Indian Institute of Technology (Banaras Hindu University)) ;
  • Rai, Richa (Department of Molecular and Human Genetics, Faculty of Science, Banaras Hindu University) ;
  • Rai, Geeta (Department of Molecular and Human Genetics, Faculty of Science, Banaras Hindu University) ;
  • Singh, Harikesh Bahadur (Department of Mycology & Plant Pathology, Institute of Agricultural Sciences, Banaras Hindu University) ;
  • Thakur, Ajit Kumar (Neuropharmacology Research Laboratory, Department of Pharmaceutics, Indian Institute of Technology (Banaras Hindu University)) ;
  • Kumar, Vikas (Neuropharmacology Research Laboratory, Department of Pharmaceutics, Indian Institute of Technology (Banaras Hindu University))
  • Received : 2014.03.20
  • Accepted : 2014.11.17
  • Published : 2014.11.30
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Abstract

Picrorhiza kurroa Royle ex Benth. (Scrophulariaceae) is a traditional Ayurvedic herb known as Kutki. It is used as a remedy for diabetes by tribes of North Eastern Himalayan region of India. Present study was conducted to explore the mechanism of antidiabetic activity of standardized aqueous extract of Picrorhiza kurroa (PkE). PkE (100 and 200 mg/kg/day) was orally administered to streptozotocin induced diabetic rats, for 14 consecutive days. Plasma insulin levels were measured and pancreas of rat was subjected to histopathological investigations. Glucose transporter type 4 (GLUT-4) protein content in the total membrane fractions of soleus muscle was estimated by Western blot analysis. Plasma insulin level was significantly increased along with concomitant increase in GLUT-4 content of total membrane fractions of soleus muscle of diabetic rats treated with extract. There was evidence of regeneration of ${\beta}$-cells of pancreatic islets of PkE treated group in histopathological examinations. PkE increased the insulin-mediated translocation of GLUT-4 from cytosol to plasma membrane or increased GLUT-4 expression, which in turn facilitated glucose uptake by skeletal muscles in diabetic rats.

Keywords

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