Search results for: PKCβ II (dn)
#32451927 
2020/05/25
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Positive interaction of mangiferin with selected oral hypoglycemic drugs: a therapeutic strategy to alleviate diabetic nephropathy in experimental rats.
Diabetic nephropathy (DN) is one of the notorious diabetes associated complications. Despite many therapeutic strategies available, metabolic control of DN continues to poses a challenge. In this study, the interactions of mangiferin with selected oral hypoglycemic drugs, metformin and gliclazide to effectively alleviate the symptoms of renal injury in DN are evaluated. Male Sprague Dawley rats were used as experimental model and type II diabetes was induced by administration of high fat diet and low dose streptozotocin. Oral intervention of mangiferin with metformin and gliclazide for a period of 28 days was given to diabetic rats. At the end of the treatment period, biochemical parameters, kidney function markers, anti-oxidant enzymes levels, oxidative stress mediated gene expression and histology were analysed. Significant reduction in the serum biochemical markers (glucose, urea and creatinine) were observed in the groups treated with combination drugs. Marked improvement in the combination treated groups in terms of inflammation and oxidative damage in the gene (TNFα, NFκB, TGFβ, VEGF, PKC) and protein expression (NFκB, VEGF) were noted in the kidney tissue alleviating the symptoms of DN. These results were further corroborated with histopathological results. Scientific data in the present study reveals that the combinations of mangiferin with the oral hypoglycemic drugs have been favorable in alleviating renal injury. Hence, a combination therapy to alleviate the vascular complication, diabetic nephropathy may be considered as a possible therapeutic strategy by including natural phytocompounds as an add on therapy to conventional oral hypoglycemic drugs.Vidhushini Sekar, Sugumar Mani, R Malarvizhi, R Barathidasan, Hannah R Vasanthi
1184 related Products with: Positive interaction of mangiferin with selected oral hypoglycemic drugs: a therapeutic strategy to alleviate diabetic nephropathy in experimental rats.
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#30516514 //
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MEDICAL BASIS OF DIABETIC NEUROPATHY FORMATION (REVIEW).
Nowadays, chronic diseases are leading cause of death worldwide. One of popular chronic disease of 21 century is Diabetes Mellitus (DM) that affected 422 million people around the world in 2014; its prevalence is expected to increase to 592 million by the year 2035. Diabetic neuropathy (DN) seems to be the most common and least understood complication being present in over 50% of chronic diabetics. As the latest date explain the pathogenesis of DN is not fully understood. Therefore, considering the widespread of DN, severity of its consequences, it is vital to investigate details of its pathophysiology and find therapeutic strategies to improve patients' condition. Generally two mechanisms have been suggested to be involved in the pathogenesis of diabetic neuropathy. The first mechanism is the activation of the Renin Angiotensin Aldosterone System (RAAS) in the presence of hyperglycemia with increased tissue level of Angiotenzin II (Ang II). Ang II stimulates Nicotin Adenine Dinucleotide (Phosphate) (NAD (P)) oxidase which enhances oxidative stress and vascular damage and leading to DN. The other mechanism is linked with disturbance in the metabolism and vasculature of nerve tissue in the presence of excessive uptake of glucose. Conclusion: In our review we have discussed different mechanisms involved in formation of DM and DN. Based on the latest research studies the main component in the big picture of DN formation is hyperglycemia.The list of mechanisms are associated with high glucose level leading inflammation, oxidative stress, hypoxia and apoptosis through the activation of several pathogenic pathways induced by Tumor Necrosis Factor alfa (TNFa), AgII, (pro)renin, Protein Kinase C (PKC), glycolysis intermediated products, Cyclooxygenase 2 (COX2) and reactive nitrogen species (RNS). Therefore to use drugs linked with above discussed pathological processes would be effective solution in the treatment of DM and its complications.A Archvadze, A Kistauri, N Gongadze, T Makharadze, K Chirakadze
2302 related Products with: MEDICAL BASIS OF DIABETIC NEUROPATHY FORMATION (REVIEW).
96 Tests1ml100ug50 assays250 g180 Tests / Kit 5 G100 Tests / Kit2001ml100ug
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#29770444 2018/05/16
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Pueraria tuberosa extract inhibits iNOS and IL-6 through suppression of PKC-α and NF-kB pathway in diabetes-induced nephropathy.
Inflammation plays an important role in the pathogenesis of diabetic nephropathy (DN). The aim of this study was to explore the anti-inflammatory role of PTY-2r (extracted from Pueraria tuberosa), on streptozotocin (STZ)-induced DN rats.Rashmi Shukla, Somanshu Banerjee, Yamini B Tripathi
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#25109475 2014/08/11
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Valsartan independent of AT₁ receptor inhibits tissue factor, TLR-2 and -4 expression by regulation of Egr-1 through activation of AMPK in diabetic conditions.
Patients suffering from diabetes mellitus (DM) are at a severe risk of atherothrombosis. Early growth response (Egr)-1 is well characterized as a central mediator in vascular pathophysiology. We tested whether valsartan independent of Ang II type 1 receptor (AT1R) can reduce tissue factor (TF) and toll-like receptor (TLR)-2 and -4 by regulating Egr-1 in THP-1 cells and aorta in streptozotocin-induced diabetic mice. High glucose (HG, 15 mM) increased expressions of Egr-1, TF, TLR-2 and -4 which were significantly reduced by valsartan. HG increased Egr-1 expression by activation of PKC and ERK1/2 in THP-1 cells. Valsartan increased AMPK phosphorylation in a concentration and time-dependent manner via activation of LKB1. Valsartan inhibited Egr-1 without activation of PKC or ERK1/2. The reduced expression of Egr-1 by valsartan was reversed by either silencing Egr-1, or compound C, or DN-AMPK-transfected cells. Valsartan inhibited binding of NF-κB and Egr-1 to TF promoter in HG condition. Furthermore, valsartan reduced inflammatory cytokine (TNF-α, IL-6 and IL-1β) production and NF-κB activity in HG-activated THP-1 cells. Interestingly, these effects of valsartan were not affected by either silencing AT1R in THP-1 cells or CHO cells, which were devoid of AT1R. Importantly, administration of valsartan (20 mg/kg, i.p) for 8 weeks significantly reduced plasma TF activity, expression of Egr-1, TLR-2, -4 and TF in thoracic aorta and improved glucose tolerance of streptozotocin-induced diabetic mice. Taken together, we concluded that valsartan may reduce atherothrombosis in diabetic conditions through AMPK/Egr-1 regulation.Yu Mi Ha, Eun Jung Park, Young Jin Kang, Sang Won Park, Hye Jung Kim, Ki Churl Chang
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#24648839 2014/02/04
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New insight into the molecular drug target of diabetic nephropathy.
Diabetic nephropathy (DN) lowered quality of life and shortened life expectancy amongst those affected. Evidence indicates interaction between advanced glycation end products (AGEs), activated protein kinase C (PKC) and angiotensin II exacerbate the progression of DN. Inhibitors of angiotensin-converting enzyme (ACEIs), renin angiotensin aldosterone system (RAAS), AGEs, and PKC have been tested for slowing down the progression of DN. The exact molecular drug targets that lead to the amelioration of renal injury in DN are not well understood. This review summarizes the potential therapeutic targets, based on putative mechanism in the progression of the disease.Vivian Soetikno, Wawaimuli Arozal, Melva Louisa, Rianto Setiabudy
2060 related Products with: New insight into the molecular drug target of diabetic nephropathy.
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#17923043 //
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[Protein kinase C-betaI, betaII in mouse diabetic nephropathy kidney and its relation to nephroprotective actions of the angiotensin receptor blocker telmisartan].
To investigate the localization and expression of protein kinase C (PKC)-betaI, betaII in diabetic nephropathy (DN) mouse kidney and its relation to angiotensin receptor blocker telmisartan (Micardis).Li-jun Yao, Jian-qing Wang, An-guo Deng, Jian-she Liu
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#17506942 //
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Effect of telmisartan on expression of protein kinase C-alpha in kidneys of diabetic mice.
To investigate the effects of angiotensin receptor blocker (ARB) telmisartan on the expression and distribution of protein kinase C (PKC)-alpha in the kidneys of diabetic mice.Li-Jun Yao, Jian-Qing Wang, Hong Zhao, Jian-She Liu, An-Guo Deng
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#17357479 //
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Different expressions of protein kinase C-alpha, beta I and beta II in glomeruli of diabetic nephropathy patients.
In current study, the expressions of protein kinase C (PKC)-alpha, beta I and beta II as well as their correlation to the expression of transforming growth factor-beta I (TGF-beta I) and vascular endothelial growth factor (VEGF) were investigated in glomeruli of normal renal tissues taken from human kidney tumors and kidney tissues from patients with diabetic nephropathy (DN). The accumulation of glomerular extracellular matrix (ECM) was determined by PAS staining, the expressions of PKC-a, PKC-beta I, PKC-beta II, TGF-beta I and VEGF were measured by semi-quantitative immunohistochemistry. Our results showed that in glomeruli of normal renal tissues, PKC-alpha and beta II had a strong expression whereas the expression of PKC-beta I was weak; in glomeruli of DN patients, the expressions of PKC-alpha, PKC-beta I, VEGF and TGF-beta I and the accumulation of ECM increased significantly, but the expression of PKC-beta II decreased markedly. Meanwhile, the expressions of PKC-alpha and beta I had a positive correlation to the expressions of VEGF and TGF-beta I respectively, whereas PKC-beta II showed no correlation to VEGF and TGF-beta I. It is concluded that the expressions of PKC-alpha, beta I and beta II in glomeruli of normal subjects and DN patients are different. PKC-alpha seems to play a critical role in human DN by up-regulating VEGF expression, whereas PKC-beta I is relatively important for the up-regulation of TGF-beta I and the accumulation of ECM under diabetic conditions.Lijun Yao, Jianqing Wang, Yan Mao, Hongyan Zhu, Anguo Deng, Zhonghua Zhu