Role of angiotensin II in the brain inflammatory events during experimental diabetes in rats

Vargas, Renata; Rincón, Jaimar; Pedreáñez, Adriana; Viera, Ninoska; Hernández-Fonseca, Juan Pablo; Peña, Caterina; Mosquera, Jesús

doi:10.1016/j.brainres.2012.03.021

Cited by 41 publications

(28 citation statements)

References 64 publications

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“…The renin-angiotensin system (RAS) contributes to the development and progression of diabetic encephalopathy as well (35). Importantly, there exists the cross-talk between the RAS and the AGE-RAGE system (36).…”

Section: Discussionmentioning

confidence: 99%

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Telmisartan Treatment Ameliorates Memory Deficits in Streptozotocin-Induced Diabetic Mice via Attenuating Cerebral Amyloidosis

Du¹,

Meng²,

Mei³

et al. 2014

J Pharmacol Sci

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Abstract. Telmisartan, an angiotensin II type 1-receptor blocker (ARBs), has been reported to exert beneficial effects on the central nervous system (CNS). However, the effect of telmisartan on cognitive impairment associated with type 1 diabetes is not well known. Here, we examined the possibility that telmisartan could improve memory function in a type 1 diabetic mouse model, streptozotocin (STZ)-induced diabetic mice. STZ-induced diabetic mice subjected to the Morris Water Maze (MWM) task exhibited a significant decline of spatial learning and memory. Oral administration of telmisartan at two nonhypotensive doses (0.7 or 0.35 mg/kg) significantly improved memory deficits in STZ-induced diabetic mice. Telmisartan treatment markedly reduced Ab 42 , APP, BACE1, RAGE, and NF-kB p65 of the hippocampus and cortex, but did not beneficially affect hyperglycemia and hypoinsulinemia in the STZ-induced diabetic mice compared with untreated diabetic mice. Taken together, our findings suggest that telmisartan ameliorates memory deficits in type 1 diabetic mice, at least partly because of attenuation of amyloidosis in the brain.

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Section: Discussionmentioning

confidence: 99%

“…It was demonstrated that AT 1 R signaling contributes to diabetes-induced neuroinflammation such as increases of angiotensin II and intercellular adhesion molecule-1 (ICAM-1), leukocyte adhesion, etc. (35,37). Angiotensin II functions as a proinflammatory factor to induce activation of the NF-kB pathway and upregulation of RAGE (36,38).…”

Section: Discussionmentioning

confidence: 99%

Telmisartan Treatment Ameliorates Memory Deficits in Streptozotocin-Induced Diabetic Mice via Attenuating Cerebral Amyloidosis

Du¹,

Meng²,

Mei³

et al. 2014

J Pharmacol Sci

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“…Losartan (LT) is an AT 1 receptor blocker that is characterized by its antioxidant defense properties during DM [7]. Moreover, LT reduced DM-induced inflammation and lipid peroxidation in diabetic rats [8]. …”

Section: Introductionmentioning

confidence: 99%

In vivo Assessment of Combined Effects of Glibenclamide and Losartan in Diabetic Rats

et al. 2018

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Objective: Diabetic complications involve multiple pathological pathways, including hyperglycemia-induced oxidative stress and inflammation. Combination therapy is usually employed to improve treatment outcomes and to lower potential adverse effects. In this study, we evaluated the effects of antidiabetic and antihypertensive agents, glibenclamide (GLI) and losartan (LT), on diabetes mellitus (DM)-associated metabolic changes in rats. Materials and Methods: Streptozotocin-induced diabetic animals were orally treated with GLI 5 mg/kg and/or LT 25 mg/kg for 4 weeks. Blood glucose, insulin, aspartate aminotransferase, alanine aminotransferase, urinary creatinine, and urea levels were measured. Serum, liver, and kidney values of inflammatory markers, such as interleukin-1β, tumor necrosis factor alpha, and interleukin-6 were assessed, along with lipid peroxidation products (e.g., thiobarbituric acid reactive substances), endogenous antioxidants (e.g., glutathione), as well as antioxidant enzyme activities (e.g., catalase, superoxide dismutase, and glutathione peroxidase). Finally, histological changes in liver and kidney tissues were evaluated. Results: DM markedly induced systemic, hepatic, and renal inflammation and lowered antioxidant defense mechanisms. Treatment of diabetic rats with either GLI or LT significantly improved liver and kidney functions and histological structure. Moreover, both medications reduced signs of oxidative stress and inflammation in blood, liver, and kidney samples. Combining GLI and LT showed similar protective potential against systemic, hepatic, and renal oxidative stress and inflammation. Conclusion: Adding LT to GLI therapy revealed prospective antioxidant and anti-inflammatory action, while no synergistic or additive effects were observed.

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“…These two factors may compromise the cardiovascular system and result in nervous damage, as well as in neuropathy development [2,14]. When these factors are settled, many symptoms may appear, like pain and tingling, which are the main characteristics of the diabetes complication process [15,16].…”

Section: Kara 2014 [11] Gynecol Endocrinolmentioning

confidence: 99%

Factors Associated With Diabetic Neuropathy In Rats: A Systematic Review With Metanalysis

Lima¹,

Vasconcelos²,

Sousa³

et al. 2017

int arch med

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Diabetic neuropathy refers to a group of symptoms associated with the nerve's damaged ability to perform its functions correctly. Symptoms may vary from paresis to pains that mainly affect sensitive or motor long nerves of feet and hands. Hence, experiments and analysis carried out with rodents, especially rats, allow several clinical interfaces to be known. Therefore, the aim of this study was to analyze the factors associated with diabetic neuropathy in rats. This is a systematic review with metanalysis. Data collection followed some prior election criteria. The sources of information for the researched data are the databases MEDLINE/PubMed and Scopus. The research was conducted using the keywords found in descriptors/MeSH: rats, diabetic neuropathies, and risk factors with the Boolean operator "AND". The BioEstat 5.3 was used for statistical analysis, and the Odds Ratio was calculated with a 95% confidence interval (CI). Eighty-three references were found, of which 17 followed the criteria and were then included in the present review. Some factors like nerve morphology, blood hypertension, oxidative stress, diabetes period, hypoglycemic effect, vascular complications, and insulin parameters represent the main risk factors for the development of diabetic neuropathy, as well as diabetes induction in rats by using drugs. Such factors are very similar to those from humans, thus requiring a deeper analysis of the theme in a considerable human sample.

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Role of angiotensin II in the brain inflammatory events during experimental diabetes in rats

Cited by 41 publications

References 64 publications

Telmisartan Treatment Ameliorates Memory Deficits in Streptozotocin-Induced Diabetic Mice via Attenuating Cerebral Amyloidosis

Telmisartan Treatment Ameliorates Memory Deficits in Streptozotocin-Induced Diabetic Mice via Attenuating Cerebral Amyloidosis

In vivo Assessment of Combined Effects of Glibenclamide and Losartan in Diabetic Rats

Factors Associated With Diabetic Neuropathy In Rats: A Systematic Review With Metanalysis

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