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Renoprotective Effect of Co-Enzyme Q10 and N-Acetylcysteine On ISSN: 2377-3634 Mahajan et al. Int J Diabetes Clin Res 2020, 7:123 DOI: 10.23937/2377-3634/1410123 Volume 7 | Issue 2 International Journal of Open Access Diabetes and Clinical Research ORIGINAL ARTICLE Renoprotective Effect of Co-Enzyme Q10 and N-Acetylcysteine on Streptozotocin-Induced Diabetic Nephropathy in Rats Manojkumar S Mahajan1*, Chandrashekhar D Upasani1, Aman B Upaganlawar1 and Vishal S Gulecha2 1Department of Pharmacology, SNJB’s Shriman Sureshdada Jain College of Pharmacy, Savitribai Phule Pune University, India 2 Check for School of Pharmaceutical Sciences, Sandip University, India updates *Corresponding author: Manojkumar S Mahajan, Assistant Professor, SNJB’s Shriman Sureshdada Jain College of Pharmacy, Savitribai Phule Pune University, India, Tel: +91-9423962663 Abstract Conclusion: The present research suggests that oxidative stress due to persistent hyperglycemia causes development Background: Persistent chronic hyperglycemia is an im- and progression of DN whereas combined administration portant player in the development and progression of diabe- of antioxidants used in the current investigation i.e. CoQ10 tic nephropathy (DN) due to generation of oxidative stress and NAC has better renoprotective effect by attenuation of (OS) which is at the center in the pathophysiology of DN DN than coenzyme Q10 or NAC alone. and underlying kidney damage. The present study was ai- med to evaluate the effect of antioxidants like Co-enzyme Keywords Q10 (CoQ10) and N-acetylcysteine (NAC) either alone or in combination in streptozotocin (STZ) induced diabetic ne- Diabetic nephropathy, Streptozotocin, Coenzyme Q10, phropathy (DN) in rats. N-acetylcysteine, Oxidative stress, Renal function Methods: Type-1 diabetes mellitus (T1DM) was induced in male Sprague-Dawley rats by intraperitoneal (i.p.) admi- Introduction nistration of 55 mg/kg STZ. DN was confirmed by asses- sment of renal function tests. Blood glucose level, glycated Diabetes mellitus (DM) is a metabolic disorders cha- hemoglobin (HbA1c), serum and urinary total protein, albu- racterized chronic hyperglycemia due to either reduced min, creatinine, urea, blood urea nitrogen (BUN) and uric glucose import and uptake resulting from decrease in acid were determined. Markers of oxidative stress including circulating levels of insulin i.e. insulin deficiency or de- superoxide dismutase (SOD), catalase (CAT), malondial- creased tissue sensitivity to it leading insulin resistance dehyde (MDA), glutathione (GSH), myeloperoxidase (MPO) and nitrite content in renal homogenate were measured. Hi- or combination of both deficiency and resistance. DM stopathological evaluation of kidney was carried to assess is categorized as type 1 (T1DM) and type 2 DM (T2DM) renal damage. The rats were treated with CoQ10 (10 mg/ [1]. Both the forms of DM possess a strong genetic com- kg, p.o.) alone or in combination with NAC (300 mg/kg, p.o.) ponent in addition to the acquired pathogenic causes. for 8 weeks after confirmation of DN. Results: Renal function of diabetic rats was significantly im- Type 1 DM which occurs due to autoimmune de- paired as indicated by renal function tests than control rats. struction of pancreatic β-cells or absolute deficiency Renal damage caused due to STZ was identified by means of insulin is also known as insulin dependent diabetes of increased MDA, depleted SOD and CAT activities and mellitus (IDDM). There is considerable evidence indi- reduced GSH. MPO activity and nitrite content in rats with cating that the chronic hyperglycemia causes many of DN increased significantly. Treatment with CoQ10 or NAC and their combined treatment improved STZ induced renal the chronic complications of DM. There are several ma- damage as reflected by reduced oxidative stress. Also, the crovascular complications like coronary artery, cerebro- combined treatment protected renal structural damage as vascular and peripheral vascular disease arising due to seen in histopathological assessment. damaged blood vessels. The primary microvascular ma- Citation: Mahajan MS, Upasani CD, Upaganlawar AB, Gulecha VS (2020) Renoprotective Effect of Co-Enzyme Q10 and N-Acetylcysteine on Streptozotocin-Induced Diabetic Nephropathy in Rats. Int J Diabetes Clin Res 7:123. doi.org/10.23937/2377-3634/1410123 Accepted: May 19, 2020: Published: May 21, 2020 Copyright: © 2020 Mahajan MS, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Mahajan et al. Int J Diabetes Clin Res 2020, 7:123 • Page 1 of 12 • DOI: 10.23937/2377-3634/1410123 ISSN: 2377-3634 nifestations of DM include diabetic nephropathy (DN), ne precursor in mammals that serves as powerful an- diabetic neuropathy and diabetic retinopathy [2,3]. tioxidant. It also shows protective action on the β-cells. NAC administration decreases hyperglycemia with the DN is a leading reason for chronic kidney disease improvement in the glucose intolerance associated (CKD) and end-stage renal disease (ESRD). It is traditio- with the glucose-induced insulin secretion [12]. NAC is nally defined as a glomerular disease inclusive of five also found beneficial in attenuating renal injury by pro- distinct stages: Glomerular hyperfiltration, incipient tecting renal structure by decreasing the apoptosis due nephropathy, microalbuminuria, overt proteinuria and to ROS. NAC is proved advantageous in patients with DN end-stage renal disease [4]. It is a progressive and irre- as it acts through dual way by reducing both hyperglyce- versible loss of renal function characterized by initial mia and renal oxidative stress [12-14]. hyperfiltration, albuminuria, glomerular mesangium expansion, accumulation of extracellular matrix, inter- Therefore, an effort was taken to study the effect stitial fibrosis, thickening of basement membranes and of antioxidants like CoQ10 and NAC in renoprotection renal cell damage. This means, DN leads to structural against experimentally induced DN. Hence, the present changes and functional abnormalities in the kidneys [5]. study was aimed to investigate the renoprotective ef- fect of CoQ10 alone and in combination with NAC in Hyperglycemia is the key player in the develop- streptozotocin (STZ) induced DN. ment of DN. Recent clinical studies have shown that persistent hyperglycemia in DM can induce oxidative Materials and Methods stress through diverse mechanisms including glucose auto-oxidation, protein glycation through non-enzyma- Drugs and chemicals tic means, polyol pathway activation and acceleration, Coenzyme Q10, as a gift sample was obtained from and reduced antioxidant defense system. Hyperglyce- Zydus Cadila, Ahmedabad, India. N-acetylcysteine was mia may act through PKC activation, acceleration of the procured from Loba Chemie (Mumbai, India). STZ was polyol pathway, production of reactive oxygen species purchased from Sigma (USA). Spectrophotometric kits (ROS) and over-expression of transforming growth fac- for assessment of superoxide dismutase (SOD), malon- tor-β (TGF-β) [6]. dialdehyde (MDA), reduced glutathione (GSH), catalase The normal kidney due to its high metabolic activity (CAT), myeloperoxidase (MPO) and nitric oxide (NO) is capable of generating a considerable oxidative stress were purchased from Elabscience Biotechnology Inc., that is balanced by an extensive antioxidant system. USA. All other Biochemical kits for estimation of total Accumulating research showed that the significant con- protein, albumin, creatinine, urea, BUN and uric acid, tributor to the diabetic complications is chronic hyper- used in the study were procured from SPAN Diagnostics, glycemia that shifts this balance to a pro-oxidant state India. All other chemicals and reagents used in the study leading to tissue damage and vascular injury [7]. It is were of analytical grade. shown that almost all pathways contributing to the DN Experimental animals induce oxidative stress by one or other mechanism. Study was conducted using adult male Sprague-Daw- Presently, the therapies used in the treatment of DN ley rats (8-weeks-old, weighing 220-250 g). Animals have not been fully efficacious due the diverse etiolo- were procured from the National Institute of Bioscien- gies in the development of DN. This results in difficulty ce, Pune and housed under standard conditions in in selecting best possible treatment strategy and thera- polypropylene cages. Rats were housed in a controlled peutic agent. Therefore effective and new therapeutic environment of temperature (18-22 °C) and light (12-hr approaches than available are needed in the treatment light/dark cycle, lights on 07:00-19:00). All animals were of DN. Many studies reported that therapies with an- given ad libitum access to standard food and water and tioxidant have a beneficial effect on DN [8]. were acclimated for 1 week prior to the beginning of the Coenzyme Q10 (ubiquinone, CoQ10), is an endo- study. All the procedures which applied to rats in this genous fat-soluble vitamin like substance serving as work were performed in accordance with ethical guide- natural antioxidant. It acts as a principal player of the lines on the care and use of animals issued by Commit- electron transport chain (ETC) of the mitochondria re- tee for the Purpose of Control and Supervision of Expe- sponsible for synthesis of ATP [9]. Apart from the pro- riments on Animals (CPCSEA). The protocol of the study ved pharmacological actions
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