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    Curcumin reduced diabetic nephropathy in a rat model
    (Funpec-Editora, 2022) Arican, C. D.; Gokdemir, G. S.; Gokdemir, M. T.; Yokus, B.; Tasdemir, E.; Sermet, A.
    This study aimed to examine the effects of curcumin, a phytochemical antioxidant, on the treatment and care of diabetic nephropathy and to contribute to alternative treatment strategies for diabetes. Male Wistar albino rats (8-10 weeks old) were divided into five groups of seven. Experimental diabetes was induced in all rats except for those in Group 1 (placebo group) by administration of 110 mg/kg nicotinamide, followed by intraperitoneal administration (after 15 min) of 55 mg/kg streptozotocin. Groups 1, 3, 4, and 5 were treated with 0.1 ml normal saline (0.9% NaCl), 150mg/kg/day metformin, 10 mg/kg/day glycazide (diamicron), and 200 mg/kg/day curcumin, respectively. Group 2 did not receive any treatment. Kidney tissues of rats were collected for histopathological examination There were no significant differences in the kidney dimensions of the rats. In the histopathological evaluation of kidney tissues with diabetic nephropathy, glomerular congestion and destruction were observed. Rats treated with curcumin had significantly less kidney damage, based on histopathological analysis, than those treated with the diabetes drugs. We conclude that curcumin has protective effects in kidneys due to its antioxidant properties. It has potential for use, in addition to antidiabetic drugs, for diabetes treatment.
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    Öğe
    Role of ghrelin in the regulation of gastric acid secretion involving nitrergic mechanisms in rats
    (Acad Sciences Czech Republic, Inst Physiology, 2008) Bilgin, H. M.; Tumer, C.; Diken, H.; Kelle, M.; Sermet, A.
    Ghrelin, an endogenous ligand for growth hormone secretagogue receptor (GHS-R), has been identified in the rat and human gastrointestinal tract. Ghrelin has been proposed to play a role in gastric acid secretion. Nitric oxide (NO) was shown as a mediator in the mechanism of ghrelin action on gastric acid secretory function. However, there is a little knowledge about this topic. We have investigated the role of ghrelin in gastric acid secretion and the role of NO as a mediator. Wistar albino rats were used in this study. The pyloric sphincter was ligated through a small midline incision. By the time, saline (0.5 ml, iv) was injected to the control group, ghrelin (20 mu g/kg, iv) was injected to the first experimental group, ghrelin (20 mu g/kg, iv) + L-NAME (70 mg/kg, sc) was injected to the second group and L-NAME (70 mg/kg, sc) was administered to the third group. The rats were killed 3 h after pylorus ligation; gastric acid secretion, mucus content and plasma nitrite levels were measured. Exogenous ghrelin administration increased gastric acid output, mucus content and total plasma nitrite levels, while these effects of ghrelin were inhibited by applying L-NAME. We can conclude that ghrelin participates in the regulation of gastric acid secretion through NO as a mediator.

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