Abstract
Background: Nephropathy is one of the serious long-term complications of diabetes. This disease is now the major single cause of end stage renal failure in many countries. Many scholars consider the genesis of DN a result of interaction of several factors, such as high glucose, oxidative stress, glycated end products (AGE), the polyol pathway and cytokines. Ginkgo Biloba has long been believed to have medicinal properties. It is among the most widely-sold herbal supplements in the world. Although the exact mechanism is unknown, evidence accumulated in vitro and in vivo shows that GB has a number of benefits, offer us a pharmacological foundation of GB for DN therapy. The aim of the current article was to investigate the possible protective effect of Ginkgo Biloba versus captopril on experimentally induced diabetic nephropathy in rats and possible mechanisms. Captopril is being used in the current study as a standard agent for comparison with Ginkgo Biloba on renoprotective effects.
Materials and Methods: Adult male albino rats were randomly divided into4 groups: group (1) normal control group. Group (2) model of diabetic nephropathy group occurred by streptozotocin 50mg/kg IP. Group (3) Ginkgo Biloba (100mg/kg /po/12weeks) treated diabetic group. Group (4) Captopril (17.5mg/kg/po/12weeks) treated diabetic group. At the end of the study period, blood samples and kidney tissues were collected and subjected to the biochemical examination (Kidney functions, AGE, oxidative stress markers and aldose reductase). In addition, histopathological examination was done on renal tissues. Results: STZ induced diabetic nephropathy, only animals with blood glucose level greater than 300mg% after 72h from STZ injected were considered diabetic. Diabetes mellitus (DM) produced a significant increase in rat kidney weight, a highly significant increase in kidney/body weight (K/B) ratio, random blood glucose, urinary albumin excretion and blood urea, serum creatinine. Also, AGE either in serum or in renal, renal, oxidative stress and aldose reductase, were significantly increased. Treatment with GB or Captopril is showing significant improvement these parameters. Histopathological pictures emphasized these results. Conclusion: GB has renoprotective effects on several pharmacological targets in progress of DN and we suggested from our study that GB is as ACE inhibitor and can be used as a first line drug to retard the progression of DN and with the use of GB we can avoid the side effects of ACE inhibitor. The therapeutic benefits may be attributed to several mechanisms include antioxidant effect. However, more studies are required to search for other benefit to GB in other diseases, its side effect and study the combination therapy between GB and captopril.
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