ABSTRACT
The aim of the study was to evaluate a possible effect of atorvastatin on renal interleukins (ILs) and prostaglandin E2 (PGE2) in type 1 diabetic rats. Thirty-two male rats from a local Wister-derived strain were included in this prospective study and were classified into four groups. Each group consisted of eight animals: Group 1, non-diabetic negative controls; Group 2, diabetic positive controls; Group 3, non-diabetic rats receiving atorvastatin for 4 weeks; and Group 4, diabetic rats receiving atorvastatin for 4 weeks. At the end of the designated period, the animals were sacrificed by cervical dislocation, and the kidneys were excised and homogenized to determine the level of IL-1ß, IL-6, IL-10, and PGE2. The study duration was from June 2015 to May 2016 at Al-Ahlyya Amman University, Amman, Jordan. In the kidneys of rats with streptozotocin-induced diabets, the levels of cytokines IL-1ß, IL-6, IL-10, and PGE2 were significantly elevated above those of the control group. This clearly showed a detrimental effect of diabetes on the kidney. Treatment of diabetic rats with atorvastatin caused a decrease in all evaluated cytokines to levels near control values. Our data suggest that atorvastatin has the potential to protect or attenuate diabetes-induced renal injury. However, the possible protective effect of atorvastatin should be supported by clinical evidence.
Subject(s)
Atorvastatin/pharmacology , Diabetes Mellitus, Experimental/metabolism , Diabetes Mellitus, Type 1/metabolism , Diabetic Nephropathies/metabolism , Dinoprostone/metabolism , Interleukin-1/metabolism , Kidney/metabolism , Tumor Necrosis Factor-alpha/metabolism , Animals , Diabetes Mellitus, Experimental/drug therapy , Diabetes Mellitus, Type 1/drug therapy , Diabetic Nephropathies/drug therapy , Male , Rats , Rats, Sprague-Dawley , Rats, WistarABSTRACT
In vitro release kinetics of three commercially available sustained release tablets (SR) diltiazem hydrochloride were studied at pH 1.1 for 2 h and for another 6 h at pH 6.8 using the USP dissolution apparatus with the paddle assemble. The kinetics of the dissolution process was studied by analyzing the dissolution data using five kinetic equations: the zero-order equation, the first-order equation, the Higuchi square root equation, the Hixson-Crowell cube root law and the Peppas equation. Analyses of the dissolution kinetic data for diltiazem hydrochloride commercial SR tablets showed that both Dilzacard and Dilzem SR tablets released drug by Non-Fickian (Anomalous transport) release with release exponent (n) equal to 0.59 and 0.54, respectively, which indicate the summation of both diffusion and dissolution controlled drug release. Bi-Tildiem SR tablets released drug by super case II (n = 1.29) which indicate zero-order release due to the dissolution of polymeric matrix and relaxation of the polymer chain. This finding was also in agreement with results obtained from application of zero-order and Hixson-Crowell equations. A dissolution profile comparative study was done to test the lyoequivelancy of the three products by using the mean dissolution time (MDT), dissimilarity factor f1 and similarity factor f2. Results showed that the three products are different and not lyoequivalent.
Subject(s)
Calcium Channel Blockers/chemistry , Diltiazem/chemistry , Technology, Pharmaceutical/methods , Chemistry, Pharmaceutical , Delayed-Action Preparations , Diffusion , Hydrogen-Ion Concentration , Kinetics , Models, Chemical , Quality Control , Solubility , TabletsABSTRACT
The major route of ammonia assimilation is the reaction which is catalyzed by glutamine synthetase to give ammonia. Cell-free extracts and purified thylakoid membranes using differential centrifugation and density gradient techniques were assayed for the percentage activity of the enzyme. Glutamine synthetase was detected in all cell-free extracts. Seventy six percent of the enzyme activity was found associated with the thylakoid membranes. Using antiserum raised to the thylakoids, 78.5% inhibition of the enzyme activity was obtained.
