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Anand Agricultural University, Anand
Anand Agricultural University (AAU) was established in 2004 at Anand with the support of the Government of Gujarat, Act No.(Guj 5 of 2004) dated April 29, 2004. Caved out of the erstwhile Gujarat Agricultural University (GAU), the dream institution of Sardar Vallabhbhai Patel and Dr. K. M. Munshi, the AAU was set up to provide support to the farming community in three facets namely education, research and extension activities in Agriculture, Horticulture Engineering, product Processing and Home Science. At present there seven Colleges, seventeen Research Centers and six Extension Education Institute working in nine districts of Gujarat namely Ahmedabad, Anand, Dahod, Kheda, Panchmahal, Vadodara, Mahisagar, Botad and Chhotaudepur
AAU's activities have expanded to span newer commodity sectors such as soil health card, bio-diesel, medicinal plants apart from the mandatory ones like rice, maize, tobacco, vegetable crops, fruit crops, forage crops, animal breeding, nutrition and dairy products etc. the core of AAU's operating philosophy however, continues to create the partnership between the rural people and committed academic as the basic for sustainable rural development. In pursuing its various programmes AAU's overall mission is to promote sustainable growth and economic independence in rural society. AAU aims to do this through education, research and extension education. Thus, AAU works towards the empowerment of the farmers.
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ThesisItem Open Access STUDIES ON AMELIORATING POTENTIAL OF CURCUMA LONGA AND PHYLLANTHUS EMBUCA ON POTASSIUM OXONATE INDUCED GOUT IN RATS(AAU, Anand, 2014) SARVAIYA, VAIDEHIBEN NITESHKUMAR; Thaker, A. M.Gout is a metabolic disorder of purine metabolism characterized by hyperuricemia (urate levels >6.8 mg/dl) and recurring attacks of arthritis and in later stages chronic arthritis, tophi formation and a tendency to renal failure. The present study was conducted to evaluate anti-gout effects of aqueous and alcoholic extracts of Curcuma longa and Phyllanthus emblica following repeated oral administration for 28 days in potassium oxonate induced hyperuricemic rats. The study was conducted on sixty six (66) male Sprague-Dawely rats dividing them in various groups having six rats in each group. Group I served as vehicle control and received the glycerin solution dissolved in water orally for 28 days of dosing period. Group II served as gout control group. Rats of group III, IV, V, VI, VII, VIII, IX, X and XI received Potassium oxonate at the dose rate of 250 mg/kg body weight, intraperitoneally every day throughout the study period for induction of gout. Group III received standard drug allopurinol orally at dose of 5 mg/kg of body weight (p.o.) for 28 days of dosing period. Group IV and V received aqueous extracts of C. longa at dose of 200 and 400 mg/kg, VI and VII received alcoholic extracts of C. longa at dose of 200 and 400 mg/kg, group VIII and IX received aqueous extracts of P. emblica at dose of 200 and 400 mg/kg and group X and XI received alcoholic extracts of P. emblica at dose of 200 and 400 mg/kg (p.o.) respectively for 28 days of dosing period. Animals were observed daily for clinical signs and mortality, if any. Body weight and feed consumption were recorded at weekly interval. On 29th day of study, animals were subjected to blood collection; blood and serum sample were analyzed for haematological and biochemical parameters respectively. At the end of study period, animals were sacrificed and necropsy was performed; tissues (kidney, liver, spleen, heart, lungs) were collected for histopathological studies. Gout rat model was developed by intra-peritoneal injection of potassium oxonate at the dose rate of 250 mg/kg body weight throughout the study period (28 days). In this gout rat model serum concentration of creatinine, uric acid, blood urea nitrogen and xanthine oxidase enzyme level was increased as compared to rats of vehicle control group. Gout control rats treated with Potassium oxonate at 250 mg/kg body weight demonstrated dull, depressed and anorectic changes along with reduced body weight gain and sluggishness in the last week of experiment. Non significant reduction in feed consumption and body weight gain were observed in gout control rats as compared to vehicle control rats at 28th day of experiment. At the end of experiment, hyperuricemic rats receiving aqueous and alcoholic extracts of C. longa and P. emblica at doses of 200 and 400 mg/kg and allopurinol at dose rate of 5 mg/kg body weight showed increase feed consumption and body weight gain as compared to rats of gout control group. Group of rats which were administrered aqueous and alcoholic extracts of C. longa showed significant increase in feed consumption in 3rd week of experiment and group of rats which were administered aqueous and alcoholic extracts of P. emblica showed significant increase in feed consumption in 1st and 2nd week of experiment. Intra-peritoneal injection of potassium oxonate increased kidney: body weight ratio in rats of gout control group as compared to vehicle control group and other treatment groups which were administered standard drug allopurinol at dose rate of 5 mg/kg body weight and aqueous and alcoholic extracts of C. longa and P. emblica at doses of 200 and 400 mg/kg body weight after 28 days of study period. Significant thrombocytosis has been noticed in gout control rats treated with potassium oxonate at 250 mg/kg body weight. While administration of aqueous and alcoholic extracts of C. longa and P. emblica at doses of 200 and 400 mg/kg and allopurinol at dose rate of 5 mg/kg body weight in hyperuricemic rats showed significant reduction in mean platelets counts as compared to gout control rats. Daily oral administration of allopurinol at 5 mg/kg body weight and aqueous and alcoholic extracts of C. longa and P. emblica at dose rate of 200 and 400 mg/kg body weight in hyperuricemic rats for 28 days produced significant reduction in serum uric acid, creatinine, blood urea nitrogen and xanthine oxidase enzyme level in dose dependent manner. Rats of gout control group showed pale kidneys grossly as compared to kidneys of vehicle control group. Microscopically, group of gout control rats receiving intra-peritoneal injections of potassium oxonate at dose rate of 250 mg/kg body weight everyday throughout the study period, showed deposition of urate crystals in renal parenchyma, atrophy of glomeruli and desquamation of tubular epithelium, severe congestion and hemorrhage with degeneration and necrosis of renal tubular epithelium and presence of proteinacious cast in renal tiibular lumen. Histological examination of sections of liver of rat from gout control group showed degeneration of hepatocytes and focal necrosis surrounded by infiltration of mononuclear cells and showed sinusoidal congestion in liver hepatocytes. On histopathological examination, sections of spleen of gout control rats showed mild congestion and hemorrhage with multifocal area of necrosis. Treatment of hyperuricemic rats with aqueous and alcoholic extracts of C. longa and P. emblica at dose rate of 200 and 400 mg/kg body weight and standard treatment allopurinol at dose rate of 5 mg/kg body weight almost preserved normal histoarchitecture of all the organs as compared to rats of gout control group. The hypouricemic effect of allopurinol, as a reference drug on reducing serum biochemical parameters was more potent and significant as compared to plant extracts treatment and reduced them upto the normal level. Aqueous and alcoholic extracts of C. longa rhizomes and fruits of P. emblica showed their effectiveness in dosedependent manner. Aqueous and alcoholic extracts of both the plants at the dose rate of 400 mg/kg body weight showed better effect and it was significantly different than dose rate of 200 mg/kg body weight. The antigout activity of C. longa and P. emblica may be due to the presence of phytochemical constituents such as phenolic compounds, plant sterols, long chain fatty acids and to a lesser extent unsaturated fatty acids. Further investigation to define its clinical efficacy would be highly desirable.ThesisItem Open Access SUB-ACUTE ORAL TOXICITY STUDY OF ATORVASTATIN ALONE AND IN COMBINATION WITH VERAPAMIL FOLLOWING REPEATED ADMINISTRATION IN HYPERLIPIDEMIC RATS(AAU, Anand, 2012) PATEL, JAYESHKUMAR BACHUBHAI; Thaker, A. M.Atorvastatin, a second-generation potent inhibitor of 3-Hydroxy 3- Methylglutaryl coenzyme A reductase is indicated for the treatment of dyslipidemia. The present study was conducted to evaluate the toxicity potential of Atorvastatin alone and in combination with Verapamil in hyperlipidemic rats. The study was conducted on 48 male Wistar rats dividing them in various groups having six rats in each group. Group I served as vehicle control and received 1.0 ml of 0.5% sodium bicarbonate solution orally for 28 days of dosing period. Group II served as hyperlipidemic control. Atorvastatin was given orally at dose rate of 0.5, 2.5 and 5.0 mg/kg body weight in poloxamer-407 induced hyperlipidemic rats of group III, IV and V respectively. Poloxamer-407 induced hyperlipidemic rats of group VI, VII and VIII received Atorvastatin at dose rate of 0.5, 2.5 and 5.0 mg/kg body weight respectively and additionally received Verapamil orally at dose rate of 10 mg/kg body weight. Animals were observed daily for clinical signs and mortality, if any. Body weight and feed consumption were recorded at weekly interval. On 29th of study, animals were subjected to blood collection; blood and serum sample were analyzed for haematological and biochemical parameters respectively. At the end of study period, animals were sacrificed and necropsy was performed; tissues (cerebrum, cerebellum, lung, liver, kidney, heart, aorta, spleen and muscle) were collected for histopathological studies. Hyperlipidemic rat model was developed by intra-peritoneal injection of poloxamer-407 at the dose rate of 500 mg/kg body weight on day prior to start of study and subsequently at every third day throughout the study period. In this dyslipidemic rat model serum concentration of triglycerides, total cholesterol and low density lipoprotein cholesterol level was increased by 15.1, 5.2 and 8.7 fold respectively; whereas high density lipoprotein cholesterol level was decreased by 1.5 fold as compared to vehicle control rats. Hjperlipidemic rats treated with Atorvastatin alone at 5.0 mg/kg body weight and in combination with Verapamil at 10 mg/kg body weight demonstrated hunched posture and piloerection along with dullness and sluggishness in the last week of experiment. Feed consumption was significantly reduced in hyperlipidemic rats treated with Atorvastatin at doses of 2.5 and 5.0 mg/kg body weight in combination with Verapamil at 10 mg/kg body weight in 3rd and 4th week of experiment. During 3rd and 4th week of study, there was also significant reduction in body weight gain of hyperlipidemic rats treated with Atorvastatin at doses of 2.5 and 5.0 mg/kg body weight in combination with Verapamil at 10 mg/kg body weight Significant neutrophilia, thrombocytopenia and lymphocytopenia have been observed in hyperlipidemic rats treated with Atorvastatin at 5.0 mg/kg body weight in combination with Verapamil at 10 mg/kg body weight. Atorvastatin alone at 2.5 and 5.0 mg/kg body weight and in combination with Verapamil at 10 mg/kg body weight produced significant hypotriglyceridemia in dyslipidemic rats. Atorvastatin alone at 5.0 mg/kg body weight and in combination with Verapamil at 10 mg/kg body weight; and Atorvastatin at 2.5 mg/kg body weight in combination with Verapamil at 10 mg/kg body weight produced significant hypocholesterolemia in dyslipidemic rats. Daily oral administration of Atorvastatin alone at 2.5 and 5.0 mg/kg body weight and in combination with Verapamil at 10 mg/kg body weight for 28 days produced significant reduction in low density lipoprotein cholesterol and significant rise in high density lipoprotein cholesterol in dyslipidemic rats. Aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and total bilirubin level were significantly increased in hyperlipidemic rats treated with Atorvastatin alone at 2.5 and 5.0 mg/kg body weight and in combination with Verapamil at 10 mg/kg body weight. Daily oral administration of Atorvastatin alone at 5.0 mg/kg body weight; at 2.5 and 5.0 mg/kg body weight in combination with Verapamil at 10 mg/kg body weight for 28 days caused significant rise in serum creatinine level in hyperlipidemic rats. Atorvastatin alone at 5.0 mg/kg body weight and in combination with Verapamil at 10 mg/kg body weight; and Atorvastatin at 2.5 mg/kg body weight in combination with Verapamil at 10 mg/kg body weight caused significant elevation in serum creatine kinase and lactate dehydrogenase level in hyperlipidemic rats. Rats of all treatment groups along with hyperlipidemic control group showed pale liver grossly. In poloxamer-407 induced hyperlipidemic rats, Atorvastatin alone at 5.0 mg/kg body weight and in combination with Verapamil at 10 mg/kg body weight showed noticeable muscle wasting condition Microscopically, fatty changes were observed in liver sections of hyperlipidemic control rats. Microscopic changes observed in liver were necrosis of hepatocytes, mild fatty changes and mild degeneration in hyperlipidemic rats treated with Atorvastatin alone at 2.5 mg/kg body weight and in combination with Verapamil at 10 mg/kg body weight. While hyperlipidemic rats treated with Atorvastatin alone at 5.0 mg/kg body weight and in combination with Verapamil at 10 mg/kg body weight revealed multifocal areas of necrosis, congestion in sections of liver; and bile duct proliferation was evident. Skeletal muscle showed loss of striations in myofibers, segmental muscle fiber necrosis, mild mononuclear cell infiltration and focal muscle fiber necrosis in hyperlipidemic rats treated with Atorvastatin alone at 5.0 mg/kg body weight and in combination with Verapamil at 10 mg/kg body weight; and Atorvastatin at 2.5 mg/kg body weight and in combination with Verapamil at 10 mg/kg body weight. Variable extent of degenerative lesions were observed in myocardium in hyperlipidemic rats treated with Atorvastatin alone at 5.0 mg/kg body weight and in combination with Verapamil at 10 mg/kg body weight; and Atorvastatin at 2.5 mg/kg body weight and in combination with Verapamil at 10 mg/kg body weight. Kidney sections showed varying extent of degenerative and necrotic lesion in renal tubules in hyperlipidemic rats treated with Atorvastatin alone at 5.0 mg/kg body weight and in combination with Verapamil at 10 mg/kg body weight. Based on serum profile as well as microscopic lesions, it was clearly observed that Atorvastatin in combination with Verapamil exhibited pronounced hepatotoxic, myotoxic and nephrotoxic potential.