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      Nephroprotective effect of Paeonia emodi via inhibition of advanced glycation end products and oxidative stress in streptozotocin–nicotinamide induced diabetic nephropathy

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      , , * ,
      Journal of Food and Drug Analysis
      Taiwan Food and Drug Administration
      antioxidant enzyme, hyperglycemia, insulin, lipid peroxidation

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          Abstract

          The present study aimed to evaluate the effect of alcohol (PA) and hydroalcohol (PHA) extract of Paeonia emodi Royale roots in treatment of streptozotocin–nicotinamide induced diabetic nephropathy. Diabetes mellitus was induced in male Wistar rats by streptozotocin (65 mg/kg intraperitoneally) 15 minutes after nicotinamide (230 mg/kg, intraperitoneally) administration and diabetic nephropathy was assessed by measuring serum glucose, renal parameters (urea, uric acid, creatinine, and blood urea nitrogen level) and lipid profile. The rats were treated with different doses of extracts (100 mg/kg, 200 mg/kg, and 400 mg/kg) for 45 days. Oxidative stress was assessed by measuring tissue antioxidant enzymes level along with the formation of advanced glycation end-products (AGEs) in kidney. PA and PHA (400 mg/kg) produced significant attenuation in the serum glucose level (165.08 ± 3.353 mg/dL and 154.27 ± 2.209 mg/dL, respectively) as compared to control. Elevated renal parameters, lipid levels, tissue antioxidant enzymes and AGE formation were also restored in a dose-dependent manner. These findings suggest that by amelioration of oxidative stress and formation of AGEs, PA and PHA significantly inhibited the progression diabetic nephropathy in rats.

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          Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction.

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            Diabetic neuropathy: mechanisms to management.

            Neuropathy is the most common and debilitating complication of diabetes and results in pain, decreased motility, and amputation. Diabetic neuropathy encompasses a variety of forms whose impact ranges from discomfort to death. Hyperglycemia induces oxidative stress in diabetic neurons and results in activation of multiple biochemical pathways. These activated pathways are a major source of damage and are potential therapeutic targets in diabetic neuropathy. Though therapies are available to alleviate the symptoms of diabetic neuropathy, few options are available to eliminate the root causes. The immense physical, psychological, and economic cost of diabetic neuropathy underscore the need for causally targeted therapies. This review covers the pathology, epidemiology, biochemical pathways, and prevention of diabetic neuropathy, as well as discusses current symptomatic and causal therapies and novel approaches to identify therapeutic targets.
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              Animal models in type 2 diabetes research: an overview.

              Type 2 diabetes is a complex and heterogeneous disorder presently affecting more than 100 million people worldwide and causing serious socio-economic problems. Appropriate experimental models are essential tools for understanding the pathogenesis, complications, and genetic or environmental influences that increase the risks of type 2 diabetes and testing of various therapeutic agents. The animal models of type 2 diabetes can be obtained either spontaneously or induced by chemicals or dietary or surgical manipulations and/or by combination thereof. In recent years, large number of new genetically modified animal models including transgenic, generalized knock-out and tissue-specific knockout mice have been engineered for the study of diabetes. This review gives an overview on the animal models of type 2 diabetes with reference to their origin/source, characteristic features, underlying causes/mechanism(s), advantages and disadvantages to the investigators in diabetes research. In addition, it especially describes the appropriate selection and usefulness of different animal models in preclinical testing of various new chemical entities (NCEs) for the treatment of type 2 diabetes.
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                Author and article information

                Journal
                J Food Drug Anal
                J Food Drug Anal
                Journal of Food and Drug Analysis
                Taiwan Food and Drug Administration
                1021-9498
                2224-6614
                2017
                11 November 2016
                : 25
                : 3
                : 576-588
                Affiliations
                M.M. College of Pharmacy, M.M. University, Mullana-Ambala, Haryana 133207, India
                Author notes
                [* ]Corresponding author. M.M. College of Pharmacy, M.M. University, Mullana-Ambala, Haryana 133207, India. E-mail address: randhirsingh.dahiya@ 123456gmail.com (R. Singh).
                Article
                jfda-25-03-576
                10.1016/j.jfda.2016.08.009
                9328827
                28911644
                676d62dd-22e4-4d99-b232-d00cd21ff525
                © 2017 Taiwan Food and Drug Administration

                This is an open access article under the CC-BY-NC-ND license ( http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 08 March 2016
                : 22 August 2016
                : 31 August 2016
                Categories
                Original Article

                antioxidant enzyme,hyperglycemia,insulin,lipid peroxidation

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