Effects of olmesartan and imidapril on the plasma adiponectin, P-selectin, and MDA-LDL levels of diabetic nephropathy patients

Utsumi, Kouichi; Yasuda, Fumihiko; Watanabe, Yozo; Higo, Seiichiro; Hirama, Akio; Fujita, Emiko; Ueda, Kae; Mii, Akiko; Kaneko, Tomohiro; Mishina, Masayoshi; Iino, Yuichi; Katayama, Yasuo

doi:10.1016/j.cca.2011.09.024

Cited by 7 publications

(5 citation statements)

References 20 publications

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“…DN causes a number of alterations to metabolism and blood circulation, and large amounts of reactive oxygen species (ROS) and inflammatory molecules are produced (29)(30)(31). MDA is a terminal product of lipid peroxide and its expression levels may indirectly reflect the degree of cell damage (32). SOD and GSH-Px are free radical scavenging enzyme system members which serve an important role in oxidative stress and anti-oxidative stress (29)(30)(31).…”

Section: Discussionmentioning

confidence: 99%

Alteration of oxidative stress and inflammatory cytokines induces apoptosis in diabetic nephropathy

Sha

et al. 2017

Molecular Medicine Reports

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Diabetic nephropathy (DN) is one of the most significant long‑term complications in terms of morbidity and mortality for diabetic patients; however, the exact cause remains unknown. To address this, the DN model was established, and oxidative stress indexes, including malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH‑Px), and inflammatory cytokines, includinginterleukin‑6 (IL‑6), tumor necrosis factor‑alpha (TNF‑α) and transforming growth factor‑beta (TGF‑β), were examined by ELISA. Renal pathological alterations and cell apoptosis was examined by hematoxylin and eosin and terminal deoxynucleotidyl transferase mediated dUTP nick‑end labeling staining, respectively. The expression levels of B‑cell lymphoma‑2 (Bcl‑2), Bcl‑2 associated X (Bax) and caspase‑3 wereexamined by immunohistochemistry and western blotting. The DN model was correctly established, with lower body weight and the higher blood glucose in the diabetes model group. The expression levels of SOD and GSH‑Px were significantly decreased in the diabetes model group; however, MDA, IL‑6, TNF‑α and TGF‑β were significantly increased. The kidney was severely damaged in the diabetes model group, with inflammatory cell invasion, increasing amount of interstitial matrix and hypertrophy with vacuolar degeneration of renal tubular cells. Cell apoptosis levels were significantly increased, and Bcl‑2 was significantly decreased in the diabetes model group in contrast with that of the sham group; however, Bax and caspase‑3 were significantly increased. It suggested that increased oxidative stress and inflammatory cytokines may enhance the apoptosis levels in DN, and may provide a significant diagnostic reference for DN in diabetes patients.

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Section: Discussionmentioning

confidence: 99%

Alteration of oxidative stress and inflammatory cytokines induces apoptosis in diabetic nephropathy

Sha

et al. 2017

Molecular Medicine Reports

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“…It has a special double-chain domain that makes it an effective antihypertensive agent when compared with the other ARBs. Similar to telmisartan, treatment with olmesartan has also increased adiponectin levels and this might improve insulin sensitivity and produce anti-atherogenic and anti-inflammatory effects in patients with diabetic nephropathy [8]. There are reports for its adverse events such as sprue-like enteropathy and mortality risk.…”

Section: Olmesartanmentioning

confidence: 96%

Angiotensin receptor blockers: Focus on cardiac and renal injury

Arumugam

Sreedhar

Thandavarayan

et al. 2016

Trends in Cardiovascular Medicine

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“…In T1DM patients, increased E-selectin plasma levels have been reported, correlating with the decline of renal function and cardiovascular risk [100]. In the case of P-selectin, T2DM patients showed increased levels of P-selectin and associated to the severity of disease [101], an effect that was reduced with the combination of ARB olmesartan and the ACEi imidapril [102].…”

Section: Cell Adhesion Moleculesmentioning

confidence: 99%

Pathogenic Pathways and Therapeutic Approaches Targeting Inflammation in Diabetic Nephropathy

Rayego‐Mateos

Morgado‐Pascual

Opazo-Ríos

et al. 2020

IJMS

174

127

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Diabetic nephropathy (DN) is associated with an increased morbidity and mortality, resulting in elevated cost for public health systems. DN is the main cause of chronic kidney disease (CKD) and its incidence increases the number of patients that develop the end-stage renal disease (ESRD). There are growing epidemiological and preclinical evidence about the close relationship between inflammatory response and the occurrence and progression of DN. Several anti-inflammatory strategies targeting specific inflammatory mediators (cell adhesion molecules, chemokines and cytokines) and intracellular signaling pathways have shown beneficial effects in experimental models of DN, decreasing proteinuria and renal lesions. A number of inflammatory molecules have been shown useful to identify diabetic patients at high risk of developing renal complications. In this review, we focus on the key role of inflammation in the genesis and progression of DN, with a special interest in effector molecules and activated intracellular pathways leading to renal damage, as well as a comprehensive update of new therapeutic strategies targeting inflammation to prevent and/or retard renal injury.

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Effects of olmesartan and imidapril on the plasma adiponectin, P-selectin, and MDA-LDL levels of diabetic nephropathy patients

Cited by 7 publications

References 20 publications

Alteration of oxidative stress and inflammatory cytokines induces apoptosis in diabetic nephropathy

Alteration of oxidative stress and inflammatory cytokines induces apoptosis in diabetic nephropathy

Angiotensin receptor blockers: Focus on cardiac and renal injury

Pathogenic Pathways and Therapeutic Approaches Targeting Inflammation in Diabetic Nephropathy

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