Effect of age receptor blocker and/or anti-inflammatory coadministration in relation to glycation, oxidative stress and cytokine production in stz diabetic rats

Elseweidy, Mohamed M.; Elswefy, Sahar E; Ameen, Rawia S.; Hashem, Reem M.

doi:10.1006/phrs.2002.0979

Cited by 27 publications

(22 citation statements)

References 41 publications

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“…AGEs may also act via the interaction with their specific receptor in cells, including cells in the immune system, and result in the generation of proinflammatory cytokines and peroxides [130]. This was confirmed in STZ-DM rats, in which the elevation of peripheral concentrations of interleukin-1b and tumor necrosis factor-a was significantly inhibited after the administration of aminoguanidine, an inhibitor of the formation of AGEs [131]. The secretion of glycated insulin from pancreatic b-cells in diabetes was recently reported [132], which may provide an explanation for the decreased biological activity of insulin in diabetes.…”

Section: Antiglycative Effects Of Garlic In Diabetesmentioning

confidence: 56%

Does garlic have a role as an antidiabetic agent?

Liu

Sheen

Lii

2007

Molecular Nutrition Food Res

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Diabetes affects a large segment of the population worldwide, and the prevalence of this disease is rapidly increasing. Despite the availability of medication for diabetes, traditional remedies are desirable and are currently being investigated. Garlic (Allium sativum), which is a common cooking spice and has a long history as a folk remedy, has been reported to have antidiabetic activity. However, there is no general agreement on the use of garlic for antidiabetic purposes, primarily because of a lack of scientific evidence from human studies and inconsistent data from animal studies. The validity of data from previous studies of the hypoglycemic effect of garlic in diabetic animals and the preventive effects of garlic on diabetes complications are discussed in this review. The role of garlic as both an insulin secretagogue and as an insulin sensitizer is reviewed. Evidence suggests that garlic's antioxidative, antiinflammatory, and antiglycative properties are responsible for garlic's role in preventing diabetes progression and the development of diabetes-related complications. Large-scale clinical studies with diabetic patients are warranted to confirm the usefulness of garlic in the treatment and prevention of diabetes.

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Section: Antiglycative Effects Of Garlic In Diabetesmentioning

confidence: 56%

Does garlic have a role as an antidiabetic agent?

Liu

Sheen

Lii

2007

Molecular Nutrition Food Res

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“…Circulating TNF-a levels have previously been reported to be elevated in diabetic patients and streptozotocininduced diabetic rats (El-Seweidy et al 2002, Jain et al 2002 and this cytokine is implicated in activation of the extrinsic cell death pathway (Gupta 2001), apoptosis during diabetes (Chen & Goeddel 2002), and apoptosis of lactotrophs (Candolfi et al 2002). However, circulating TNF-a levels were increased as early as 1 week after the onset of diabetes, while caspase-8 activation and increased cell death was not detected until the fourth week.…”

Section: Discussionmentioning

confidence: 98%

“…Caspase-8 is the prototypical caspase of the extrinsic or death receptor pathway of apoptosis that is activated by an extracellular insult or ligand binding to members of the tumor necrosis factor (TNF)-a receptor superfamily (Boldin et al 1996, Wajant 2002. Indeed, circulating TNF-a levels are reported to be elevated in diabetic patients, as well as in streptozotocin-induced diabetic rats (El-Seweidy et al 2002, Jain et al 2002, and this cytokine is implicated in apoptosis during diabetes (Chen & Goeddel 2002) and in lactotrophs (Candolfi et al 2002), suggesting its possible involvement in the loss of this cell type in diabetes.…”

Section: Introductionmentioning

confidence: 99%

Increased apoptosis of lactotrophs in streptozotocin-induced diabetic rats is followed by increased proliferation

Arroba

Frago

Argente

et al. 2006

Journal of Endocrinology

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Poorly controlled diabetes mellitus can result in decreased prolactin production and thus problems with lactation, reproduction, and other physiological processes. This may be due to a loss of lactotrophs, as we have previously shown that long-term (8 weeks) poorly controlled streptozotocininduced diabetes results in increased death of lactotrophs and that this most likely occurs through the activation of caspase-8 and the extrinsic cell death cascade. However, cell proliferation is also increased in the anterior pituitary at this time, although the cell type undergoing this proliferation and whether it is a response to the increased cell death remains unknown. In order to determine the time-course of increased cell death and proliferation in the anterior pituitary and if this is related to changes in tumor necrosis factor (TNF)-a, a cytokine involved in the activation of the extrinsic cell death pathway, rats were killed at 1, 4, 6, and 8 weeks after the induction of diabetes. Cell death was significantly increased after 4 weeks, as was caspase-8 activation, although circulating levels of TNF-a were increased as early as 1 week. Pituitary levels of TNF-a did not change significantly until 8 weeks after diabetes onset. Similarly, Western-blot analysis of proliferating cell nuclear antigen showed that anterior pituitary cell proliferation increased significantly 8 weeks after diabetes onset, with the majority of proliferating cells, as detected by BrdU incorporation, corresponding to lactotrophs. These results suggest that the increased death of lactotrophs in poorly controlled diabetic rats is followed by increased proliferation of this cell type, even when no treatment is given.

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“…2. Omega-3 fatty acids (Super omega Ò ), soft gelatin capsules containing 50% polyunsaturated fatty acids (eicosapentaenoic acid and decosahexaenoic acid): the oil was suspended in gum acacia, given orally daily for 3 weeks at a dose of 12 mg/kg body weight using oral gavage [17,18]. 3.…”

Section: Animals and Treatmentmentioning

confidence: 99%

Effect of Some Natural Products Either Alone or in Combination on Gastritis Induced in Experimental Rats

et al. 2008

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Gastritis, an inflammatory state in gastric mucosa, can be induced experimentally in various ways. The present study considered the iodoacetamide model (Iodo). Omega-3 fatty acids (fish oil), black seed oil, and curcuminoids (natural products) in addition to omeprazole (synthetic proton-pump inhibitor) were tested. Supplementation of 0.1% iodoacetamide to drinking water of experimental rats for two consecutive weeks resulted in: (i) increased serum nitric oxide (NO) and gastrin, and decreased pepsinogen, (ii) depletion of gastric mucosal glutathione (GSH), and (iii) increased gastric mucosal lipid peroxidation (MDA), but failed to affect gastric mucosal myeloperoxidase (MPO) activity. Histological examination showed marked neutrophilic infiltration after 1 week of iodoacetamide administration and shedding of apical cell layer with pale edematous vacuolated gastric gland cells and thickening of muscularis mucosa after 2 weeks of iodoacetamide intake. Individual administration of omega-3 fatty acids 12 mg/kg, black seed oil 50 mg/kg, and curcuminoids 50 mg/kg body weight orally daily for 3 weeks decreased MDA, gastrin, and NO, and normalized mucosal GSH but failed to affect serum pepsinogen level. Combined administration of these natural products for 3 weeks normalized MPO activity, and other effects were nearly the same as with individual use. Omeprazole administration 30 mg/kg body weight orally daily for 3 weeks induced a similar response except for an observed increase in serum gastrin and pepsinogen levels.

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Effect of age receptor blocker and/or anti-inflammatory coadministration in relation to glycation, oxidative stress and cytokine production in stz diabetic rats

Cited by 27 publications

References 41 publications

Does garlic have a role as an antidiabetic agent?

Does garlic have a role as an antidiabetic agent?

Increased apoptosis of lactotrophs in streptozotocin-induced diabetic rats is followed by increased proliferation

Effect of Some Natural Products Either Alone or in Combination on Gastritis Induced in Experimental Rats

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