Hanan H Hagar
King Saud University, KSA
Hanan H Hagar, B Pharm, MS, PhD, is a Professor of Pharmacology in Medical College, King Saud University. She received her BPharm degree (Excellent with honors) from Zagazig University, Egypt. She completed her MPharm degree from Zagazig University, Egypt and PhD from Zagazig University in collaboration with University of Arkansas for Medical Sciences, USA. She usually has excellent evaluation and Deanship of Quality. She is a member of many societies and a Member of Advisory Board for many international journals liek Saudi Pharmaceutical Journal, Dataset Papers of Pharmacology, Hindawi Publishing Corporation, SciTz Medical and Clinical Toxicology, Journal of Nutrition & Food Sciences, JSM Renal Medicine and SRL Nephrology & Therapeutics. She served also as invited reviewer for many national and international journals worldwide as Urological Research (UK); Clinica Chimica Acta (Netherlands); Cell & Tissue Transplantation & Therapy (New-zeland); Digestive Diseases and Sciences (Netherlands) and Acta Pharmacologica Sinica (China). She had actively participated in many local and international conferences as poster or oral presentation. She was invited as a speaker in many conferences. She has published over 30 research articles in peer reviewed ISI international journals. She has been awarded for many projects by many financial sources. These projects were funded by different organizations as King Abdul Aziz City for Science and Technology (KACST), Saudi Arabia; Research Center at Women Students-Medical Studies & Sciences Sections, King Saud University; Research Center at College of Medicine, King Saud University and Saudi Arabia Basic Industries Corporation (SABIC). Due to her scientific record, she was included in the 2009-2010 Edition of "Who's Who in Medicine and Healthcare", the American biographical works “Great Minds of the 21st Century”, 2010 England and “Woman of the year in Medicine and Health care”, 2010.
Implication of oxidative stress and inflammatory mechanisms in adriamycin nephropathy has been suggested. Reactive oxygen species may activate latent matrix metalloproteinases (MMP) that ultimately may induce glomerulosclerosis and fibrosis. Little is known about the effect of MMP inhibitors on focal segmental glomerulosclerosis. This study examined the role of MMP in adriamycin nephropathy as an animal model of glomerulosclerosis using MMP inhibitors, SB-3CT and doxycycline. Forty (40) male Wistar rats were used and allocated into four groups as follows: Normal control rats (n=10), adriamycin treated rats (n=10) and SB-3CT+adriamycin-treated rats (n=10), doxycycline+adriamycin-treated rats (n=10). Adriamycin nephropathy was induced by a single injection of adriamycin (7.5 mg/kg) intraperitoneally. SB-3CT was given at a dose of (1 mg/kg/day, i.p.) while doxycycline was given at a dose of (30 mg/kg/day, i.p.). Therapy was initiated at once after induction of adriamycin nephropathy and continued for 4 weeks. Adriamycin nephropathy resulted in deterioration in lipid profile (elevated serum triglycerides and cholesterol levels) and in kidney function (elevated serum creatinine, BUN) and reduction in serum albumin and total protein levels while their levels were increased in urine. Lipid profile was also changed. Adriamycin-treated rats showed increased tumor necrosis factor-α (TNF-α); intercellular adhesion molecule-1 (ICAM-1), transforming growth factor-b1 and tissue inhibitor of metalloproteinase-1 and 2 (TIMP-1 and TIMP-2) in the kidney as assessed by ELISA technique. MMP activities (MMP-2 and MMP-9) were also induced using zymography technique and western blot analysis. Histological changes were also noted on kidney using hematoxylin and eosin. Immunohistochemical studies revealed increased staining of collagen IV in the renal cortex. MMP inhibitors, doxycycline and SB-3CT significantly reduced serum BUN, creatinine and renal cytokines. Lipid abnormalities were also corrected back to normal. This was parallel to reduction in collagen IV immunostaining and improvement in histological changes. These results suggested that MMP inhibitors may have promise as anti-inflammatory, anti-proliferative and endothelial cell protective. MMP inhibitors may be potential future candidates to provide more effective therapy to halt the development of glomerulosclerosis.