Shri Gopi Chand Group of Institutions

Bāghpat, India

Shri Gopi Chand Group of Institutions

Bāghpat, India

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Rohilla A.,Shri Gopi Chand Group of Institutions
Pharmacological Research | Year: 2010

Aminoglycoside antibiotics are employed clinically because of their potent bactericidal activities, less bacterial resistance, post-antibiotic effects and low cost. However, drugs belong to this class are well-known to cause nephrotoxicity, which limits their frequent clinical exploitation. Gentamicin, a commonly used aminoglycoside, is associated with an induction of tubular necrosis, epithelial oedema of proximal tubules, cellular desquamation, tubular fibrosis, glomerular congestion, perivascular edema and inflammation, which ultimately show the way to renal dysfunction. It is a matter of debate whether we have promising agents to prevent the incidence of gentamicin-induced nephrotoxicity. The present review critically discussed the pathogenesis of gentamicin-induced nephrotoxicity. In addition, based on the experimental and clinical studies, the possible therapeutic approach to prevent gentamicin-induced nephrotoxicity has been discussed. © 2010 Elsevier Ltd.


Rohilla A.,Shri Gopi Chand Group of Institutions | Omer N.,Shri Gopi Chand Group of Institutions | Kushnoor A.,Shri Gopi Chand Group of Institutions
International Journal of Pharmacy and Technology | Year: 2012

Diabetic cardiomyopathy (DCM) is a complication of disease associated with coronary artery disease (CAD) and myocardial dysfunction in diabetic patients. Various metabolic perturbations are involved in DCM that include depletion of glucose transporter-4 (GLUT-4), increase of free fatty acids (FFAs), microvascular changes and structural and functional changes in myocardium. A number of signaling mechanisms are involved in the pathogenesis of DCM like metabolic disturbances, myocardial fibrosis, small vessel disease, autonomic dysfunction and insulin resistance. In addition, other molecular factors involved in DCM like reactive oxygen species (ROS), nitric oxide (NO), poly(ADP-ribose) polymerase (PARP), protein kiase C (PKC) and advanced glycation end products (AGEs) have been implicated in the pathogenesis of DCM. This review article seeks to evaluate the evidence for the existence of DCM, clarify the potential signaling mechanisms responsible and possible therapeutic implications for the treatment of DCM.


Rohilla A.,Shri Gopi Chand Group of Institutions | Singh V.,Shri Gopi Chand Group of Institutions | Kushnoor A.,Shri Gopi Chand Group of Institutions
International Journal of Pharmacy and Technology | Year: 2012

Diabetic neuropathy (DN) has been considered as one of the most frequent and troublesome complications of diabetes mellitus. It is the foremost cause of morbidity and mortality among diabetic patients worldwide. In addition, it has been frequently associated with devastating pain. However, the complete knowledge of the history and pathogenesis of the disease remains limited but several mediators have been reported to be involved in the pathogenesis of DN that involve polyol pathway, increased formation of advanced glycation end products (AGEs), enhanced reactive oxygen species (ROS) generation and activation of protein kinase C (PKC). Moreover, management of patients presented with DN has been done by both pharmacological and non-pharmacological strategies. The review critically explains about the pathogenesis and treatment strategies available for the DN.

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