Houttuynia cordata aqueous extract attenuated glycative and oxidative stress in heart and kidney of diabetic mice
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The anti-glycative and anti-oxidative effects from Houttuynia cordata leaves aqueous extract (HCAE) in heart and kidney of diabetic mice were examined.
HCAE, at 1 or 2 %, was supplied in drinking water for 8 weeks. Plasma glucose and blood urea nitrogen (BUN) levels and creatine phosphokinase (CPK) activity were measured. The production of oxidative and inflammatory factors was determined. Activity and protein expression of associated enzymes or regulators were analyzed.
HCAE intake at both doses lowered plasma glucose and BUN levels, and CPK activity and also restored creatinine clearance rate in diabetic mice. HCAE intake, only at 2 %, retained plasma insulin levels (P < 0.05). HCAE reduced reactive oxygen species, protein carbonyl, interleukin-6, tumor necrosis factor-alpha, N ε -(carboxymethyl)-lysine, pentosidine and fructose levels, and reserved glutathione content in heart and kidney of diabetic mice (P < 0.05). Diabetes enhanced aldose reductase (AR) activity and protein expression in heart and kidney (P < 0.05). HCAE intake at both doses decreased renal AR activity and protein expression, but only at 2 % lowered cardiac AR activity and protein expression (P < 0.05). Diabetes increased protein expression of RAGE, p47phox and gp91phox, nuclear factor kappa-B (NF-κB) p50, NF-κB p65 and mitogen-activated protein kinase in heart and kidney (P < 0.05). HCAE intake only at 2 % limited RAGE expression, but at 1 and 2 % downregulated p47phox, NF-κB p65 and p-p38 expression in these organs (P < 0.05).
These findings suggest that Houttuynia cordata leaves aqueous extract could ameliorate cardiac and renal injury under diabetic condition.
KeywordsHouttuynia cordata Diabetes Glycation Polyol pathway NADPH oxidase
Advanced glycation endproducts
Blood urea nitrogen
Creatinine clearance rate
Houttuynia cordata leaves aqueous extract
Mitogen-activated protein kinase
Nuclear factor kappa-B
Relative fluorescence unit
Reactive oxygen species
Tumor necrosis factor-alpha
This study was partially supported by a Grant from Ministry of Science and Technology, Taipei City, Taiwan (NSC 102-2313-B-039-002-MY3).
Compliance with ethical standards
Conflict of interest
There was no conflict of interest regarding this manuscript.
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