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Protective effect of S-allylcysteine against cyclophosphamide-induced bladder hemorrhagic cystitis in mice
Authors:Kanchan Bhatia  Firoz Ahmad  Hina Rashid  Sheikh Raisuddin
Affiliation:1. Department of Medical Elementology and Toxicology, Hamdard University, New Delhi 110 062, India;2. Department of Internal Medicine, UT Southwestern Medical Center, Dallas, TX 75390, USA
Abstract:S-Allylcysteine (SAC), an organosulfur compound of aged garlic extract (AGE) regulates the thiol status of the cell and scavenges free radicals. Depletion of thiols along with free radical generation has been implicated in cyclophosphamide (CP)-induced urotoxicity. We studied modulatory effect of SAC on CP-induced urotoxicity in mice focusing on hemorrhagic cystitis (HC). SAC (150 and 300 mg kg−1) was administered in CP treated animals (200 mg kg−1) and bladder was observed for histological and biochemical changes. CP treatment caused a marked increase in the lumen exudates, edema, vasodilation and HC in lamina propia in the bladder. These changes were accompanied by increase in lipid peroxidation (LPO), and decrease in reduced glutathione (GSH) and activities of antioxidant enzymes. SAC not only showed protection in tissue histology but also improved the decreased activities of antioxidant enzymes. SAC treatment also reduced LPO and increased GSH levels. Although SAC treatment did not ensure full recovery, the marked improvement in histology and antioxidants of bladder suggests that it has a significant modulatory effect on CP-induced urotoxicity. Since decrease in antioxidant level is the major cause of CP urotoxicity, the protective effect of SAC deserves its further exploration involving laboratory and clinical investigations.
Keywords:AGE, aged garlic extract   CP, cyclophosphamide   CAT, catalase   GP, gluathione peroxidase   GR, gluathione reductase   GSH, reduced glutathione   GST, glutathione S-transferase   HC, hemorrhagic cystitis   iNOS, inducible nitric oxide synthase   IL-1β, interleukin β   LPO, lipid peroxidation   NF-κB, nuclear factor κB   OSC, organosulfur compound   ROS, reactive oxygen species S-allylcysteine   SAMC, S-allyl mercaptocysteine   SOD, superoxide dismutase   TBARS, thiobarbituric acid reactive substances   TNFα, tumor necrosis factor-α
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