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Junbo Yang - One of the best experts on this subject based on the ideXlab platform.
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Gliquidone Alleviates Diabetic Nephropathy by Inhibiting Notch/Snail Signaling Pathway.
Cellular Physiology and Biochemistry, 2018Co-Authors: Hengyu Tian, Junbo YangAbstract:Background/Aims: Diabetic Nephropathy is a common complication of diabetes. This study explored the renal protective effect and possible mechanism of gliquidone in mice with Diabetic Nephropathy. Methods: Animal model of Diabetic Nephropathy was established in KKAy mice. The renal protective effect of gliquidone was studied by evaluating the kidney function through measures of urinary protein, blood urea nitrogen (BUN), serum creatinine (Scr) and serum triglyceride (TG) that were performed using an automatic biochemical analyzer. The levels of oxidative stress indicators, such as nitric oxide (NO), superoxide dismutase (SOD) and malondialdehyde (MDA), were evaluated in renal tissue homogenates using the automatic biochemical analyzer. The inhibitory effect of gliquidone on renal interstitial fibrosis and its association with Notch / Snail1 signaling pathway in Diabetic Nephropathy was investigated using molecular biological techniques. Results: It was found that low-, medium- and high-dose gliquidone improved the mice’s general health condition, such as mental status, fur condition, eating, and drinking. Gliquidone reduced the body weight and the kidney weight /body weight ratio of mice. Gliquidone improved the kidney function, indicated by reductions in urinary protein, blood urea nitrogen, and serum creatinine and triglyceride. Gliquidone treatment increased levels of nitric oxide and superoxide dismutase, but decreased level of malondialdehyde. The expression of Jagged1/Notch1/hes1/Snail1/α-SMA decreased, while the expression of E-cadherin increased in gliquidone-treated kidneys. High dose gliquidone showed the best effect, one that was similar to that of the positive control drug irbesartan. Conclusion: Taken together, our results suggested that gliquidone can ameliorate the Diabetic symptoms of Diabetic Nephropathy through inhibiting Notch / Snail1 signaling pathway, improving anti -oxidative response and delaying renal interstitial fibrosis. The efficacy of gliquidone is dose-dependent.
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gliquidone alleviates Diabetic Nephropathy by inhibiting notch snail signaling pathway
Cellular Physiology and Biochemistry, 2018Co-Authors: Hengyu Tian, Junbo YangAbstract:Background/Aims: Diabetic Nephropathy is a common complication of diabetes. This study explored the renal protective effect and possible mechanism of gliquidone in mice with Diabetic Nephropathy. Methods: Animal model of Diabetic Nephropathy was established in KKAy mice. The renal protective effect of gliquidone was studied by evaluating the kidney function through measures of urinary protein, blood urea nitrogen (BUN), serum creatinine (Scr) and serum triglyceride (TG) that were performed using an automatic biochemical analyzer. The levels of oxidative stress indicators, such as nitric oxide (NO), superoxide dismutase (SOD) and malondialdehyde (MDA), were evaluated in renal tissue homogenates using the automatic biochemical analyzer. The inhibitory effect of gliquidone on renal interstitial fibrosis and its association with Notch / Snail1 signaling pathway in Diabetic Nephropathy was investigated using molecular biological techniques. Results: It was found that low-, medium- and high-dose gliquidone improved the mice’s general health condition, such as mental status, fur condition, eating, and drinking. Gliquidone reduced the body weight and the kidney weight /body weight ratio of mice. Gliquidone improved the kidney function, indicated by reductions in urinary protein, blood urea nitrogen, and serum creatinine and triglyceride. Gliquidone treatment increased levels of nitric oxide and superoxide dismutase, but decreased level of malondialdehyde. The expression of Jagged1/Notch1/hes1/Snail1/α-SMA decreased, while the expression of E-cadherin increased in gliquidone-treated kidneys. High dose gliquidone showed the best effect, one that was similar to that of the positive control drug irbesartan. Conclusion: Taken together, our results suggested that gliquidone can ameliorate the Diabetic symptoms of Diabetic Nephropathy through inhibiting Notch / Snail1 signaling pathway, improving anti -oxidative response and delaying renal interstitial fibrosis. The efficacy of gliquidone is dose-dependent.
Hengyu Tian - One of the best experts on this subject based on the ideXlab platform.
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Gliquidone Alleviates Diabetic Nephropathy by Inhibiting Notch/Snail Signaling Pathway.
Cellular Physiology and Biochemistry, 2018Co-Authors: Hengyu Tian, Junbo YangAbstract:Background/Aims: Diabetic Nephropathy is a common complication of diabetes. This study explored the renal protective effect and possible mechanism of gliquidone in mice with Diabetic Nephropathy. Methods: Animal model of Diabetic Nephropathy was established in KKAy mice. The renal protective effect of gliquidone was studied by evaluating the kidney function through measures of urinary protein, blood urea nitrogen (BUN), serum creatinine (Scr) and serum triglyceride (TG) that were performed using an automatic biochemical analyzer. The levels of oxidative stress indicators, such as nitric oxide (NO), superoxide dismutase (SOD) and malondialdehyde (MDA), were evaluated in renal tissue homogenates using the automatic biochemical analyzer. The inhibitory effect of gliquidone on renal interstitial fibrosis and its association with Notch / Snail1 signaling pathway in Diabetic Nephropathy was investigated using molecular biological techniques. Results: It was found that low-, medium- and high-dose gliquidone improved the mice’s general health condition, such as mental status, fur condition, eating, and drinking. Gliquidone reduced the body weight and the kidney weight /body weight ratio of mice. Gliquidone improved the kidney function, indicated by reductions in urinary protein, blood urea nitrogen, and serum creatinine and triglyceride. Gliquidone treatment increased levels of nitric oxide and superoxide dismutase, but decreased level of malondialdehyde. The expression of Jagged1/Notch1/hes1/Snail1/α-SMA decreased, while the expression of E-cadherin increased in gliquidone-treated kidneys. High dose gliquidone showed the best effect, one that was similar to that of the positive control drug irbesartan. Conclusion: Taken together, our results suggested that gliquidone can ameliorate the Diabetic symptoms of Diabetic Nephropathy through inhibiting Notch / Snail1 signaling pathway, improving anti -oxidative response and delaying renal interstitial fibrosis. The efficacy of gliquidone is dose-dependent.
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gliquidone alleviates Diabetic Nephropathy by inhibiting notch snail signaling pathway
Cellular Physiology and Biochemistry, 2018Co-Authors: Hengyu Tian, Junbo YangAbstract:Background/Aims: Diabetic Nephropathy is a common complication of diabetes. This study explored the renal protective effect and possible mechanism of gliquidone in mice with Diabetic Nephropathy. Methods: Animal model of Diabetic Nephropathy was established in KKAy mice. The renal protective effect of gliquidone was studied by evaluating the kidney function through measures of urinary protein, blood urea nitrogen (BUN), serum creatinine (Scr) and serum triglyceride (TG) that were performed using an automatic biochemical analyzer. The levels of oxidative stress indicators, such as nitric oxide (NO), superoxide dismutase (SOD) and malondialdehyde (MDA), were evaluated in renal tissue homogenates using the automatic biochemical analyzer. The inhibitory effect of gliquidone on renal interstitial fibrosis and its association with Notch / Snail1 signaling pathway in Diabetic Nephropathy was investigated using molecular biological techniques. Results: It was found that low-, medium- and high-dose gliquidone improved the mice’s general health condition, such as mental status, fur condition, eating, and drinking. Gliquidone reduced the body weight and the kidney weight /body weight ratio of mice. Gliquidone improved the kidney function, indicated by reductions in urinary protein, blood urea nitrogen, and serum creatinine and triglyceride. Gliquidone treatment increased levels of nitric oxide and superoxide dismutase, but decreased level of malondialdehyde. The expression of Jagged1/Notch1/hes1/Snail1/α-SMA decreased, while the expression of E-cadherin increased in gliquidone-treated kidneys. High dose gliquidone showed the best effect, one that was similar to that of the positive control drug irbesartan. Conclusion: Taken together, our results suggested that gliquidone can ameliorate the Diabetic symptoms of Diabetic Nephropathy through inhibiting Notch / Snail1 signaling pathway, improving anti -oxidative response and delaying renal interstitial fibrosis. The efficacy of gliquidone is dose-dependent.
Carsten Tschöpe - One of the best experts on this subject based on the ideXlab platform.
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the role of the renal kallikrein kinin system in Diabetic Nephropathy
Current Opinion in Nephrology and Hypertension, 2007Co-Authors: Alexander Riad, Jia Long Zhuo, Heinz-peter Schultheiss, Carsten TschöpeAbstract:Purpose of review Diabetic Nephropathy is one of the most common complications in diabetes mellitus. Multiple pathogenic mechanisms are now believed to contribute to this disease, including inflammatory cytokines, autacoids and oxidative stress. Numerous studies have shown that the kallikrein–kinin system may be involved in these mechanisms. This review focuses on recent research advance on the potential role of the kallikrein–kinin system in the development of Diabetic Nephropathy, and its clinical relevance.
K J Schjoedt - One of the best experts on this subject based on the ideXlab platform.
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beneficial impact of spironolactone on nephrotic range albuminuria in Diabetic Nephropathy
Kidney International, 2006Co-Authors: K J Schjoedt, Hanshenrik Parving, Kasper Rossing, Tina R Juhl, Frans Boomsma, Lise Tarnow, Peter RossingAbstract:Reduction of nephrotic range albuminuria is associated with markedly improved renal and cardiovascular outcome in patients with Diabetic Nephropathy. Aldosterone has been suggested to play a role in the progression of Diabetic Nephropathy. We therefore aimed to evaluate the short-term effect of aldosterone antagonism with spironolactone on nephrotic range albuminuria and blood pressure in Diabetic Nephropathy. Twenty Caucasian patients with Diabetic Nephropathy and nephrotic range albuminuria (>2500 mg/24 h) despite recommended antihypertensive treatment completed this double-masked, randomized crossover trial. Patients were treated in random order with spironolactone 25 mg once daily and matched placebo for 2 months, on top of ongoing antihypertensive treatment, including an angiotensin-converting enzyme inhibitor or an angiotensin II receptor blocker in maximally recommended doses. Median (range) number of antihypertensive drugs was 3 (2–5). After each treatment period, albuminuria, 24-h ambulatory blood pressure, and glomerular filtration rate (GFR) were determined. Spironolactone on top of recommended renoprotective treatment induced a 32% (95% confidence interval (CI): 21–42%) reduction in albuminuria from (geometric mean (95% CI)) 3718 (2910–4749) mg/24 h on placebo treatment ( P P 2 from 64 (27) ml/min/1.73 m 2 . No patients were excluded due to adverse events. Our results suggest that spironolactone treatment on top of recommended renoprotective treatment including maximal renin–angiotensin system blockade may offer additional renoprotection in patients with Diabetic Nephropathy and nephrotic range albuminuria.
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beneficial impact of spironolactone in Diabetic Nephropathy
Kidney International, 2005Co-Authors: K J Schjoedt, Kasper Rossing, Tina R Juhl, Frans BoomsmaAbstract:Beneficial impact of spironolactone in Diabetic Nephropathy. Background Aldosterone has been suggested to play a role in the initiation and progression of Diabetic Nephropathy. Currently recommended treatment with angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers [renin-angiotensin system (RAS) blockade] does not suppress circulating aldosterone sufficiently. We therefore aimed to evaluate the short-term effect of aldosterone antagonism with spironolactone on albuminuria and blood pressure in Diabetic Nephropathy. Methods Twenty Caucasian type 1 Diabetic patients with persistent macroalbuminuria despite antihypertensive treatment, including RAS blockade, completed this double-masked, randomized cross-over trial. Patients were treated in random order with spironolactone 25mg once daily and matched placebo for two months, respectively, on top of usual antihypertensive treatment. After each treatment period albuminuria, 24-hour blood pressure, and glomerular filtration rate (GFR) were determined. Results Spironolactone on top of usual antihypertensive treatment induced a 30% (95% CI 17 to 41) reduction in albuminuria from [geometric mean (95% CI)] 831 (624 to 1106) mg/24-hour on placebo treatment ( P P P Conclusion Our results suggest that spironolactone treatment on top of recommended antihypertensive treatment reduces blood pressure and may offer additional renoprotection in type 1 Diabetic patients with Diabetic Nephropathy.
Wei Li - One of the best experts on this subject based on the ideXlab platform.
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reversibility of structural and functional damage in a model of advanced Diabetic Nephropathy
Journal of The American Society of Nephrology, 2013Co-Authors: Warangkana Pichaiwong, Tri Q Nguyen, Kelly L Hudkins, Tomasz Wietecha, Chiraporn Tachaudomdach, Wei Li, Bardia Askari, Takahisa Kobayashi, Kevin D Obrien, Jeffrey W PippinAbstract:The reversibility of Diabetic Nephropathy remains controversial. Here, we tested whether replacing leptin could reverse the advanced Diabetic Nephropathy modeled by the leptin-deficient BTBR ob/ob mouse. Leptin replacement, but not inhibition of the renin-angiotensin-aldosterone system (RAAS), resulted in near-complete reversal of both structural (mesangial matrix expansion, mesangiolysis, basement membrane thickening, podocyte loss) and functional (proteinuria, accumulation of reactive oxygen species) measures of advanced Diabetic Nephropathy. Immunohistochemical labeling with the podocyte markers Wilms tumor 1 and p57 identified parietal epithelial cells as a possible source of regenerating podocytes. Thus, the leptin-deficient BTBR ob/ob mouse provides a model of advanced but reversible Diabetic Nephropathy for further study. These results also suggest that restoration of lost podocytes is possible but is not induced by RAAS inhibition, possibly explaining the limited efficacy of RAAS inhibitors in promoting repair of Diabetic Nephropathy.
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mangiferin prevents Diabetic Nephropathy progression in streptozotocin induced Diabetic rats
Phytotherapy Research, 2009Co-Authors: Xuan Li, Xiaodong Li, Wei LiAbstract:Diabetic Nephropathy is one of the most severe Diabetic microangiopathies and accounting for approximately one-third of all cases of end-stage renal disease. In the present study, we investigated the effect of mangiferin, a polyphenol from Anemarrhena asphodeloides Bge. or Mangifera indica L., on Diabetic Nephropathy and the possible mechanisms by using a developed Diabetic Nephropathy rat model and cultured rat mesangial cells. Serum-advanced glycation end-products level, malonaldehyde level, sorbitol concentration of red blood cell, 24 h albuminuria excretion were signifi cantly decreased, whereas activity of serum superoxide dismutase and glutathione peroxidase and creatinine clearance rate were increased by mangiferin. Blood glucose level remained unaffected. Mangiferin signifi cantly inhibited glomerular extracellular matrix expansion and accumulation and transforming growth factor-beta 1 overexpression in glomeruli of Diabetic Nephropathy rats. Moreover, mangiferin was observed to inhibit proliferation of mesangial cells induced by high glucose and the overexpression of collagen type IV of mesangial cells induced by advanced glycation end products. In summary, mangiferin could signifi cantly prevent progression of Diabetic Nephropathy and improve renal function. Copyright © 2009 John Wiley & Sons, Ltd.