AIM:To investigate the aldose reductase(AR)inhibition capacity of astragalin(AST)against streptozoticin-induced diabetic cataracts(DCs)in rats.METHODS:Ex vivo investigations were conducted by treating the lens of a go...AIM:To investigate the aldose reductase(AR)inhibition capacity of astragalin(AST)against streptozoticin-induced diabetic cataracts(DCs)in rats.METHODS:Ex vivo investigations were conducted by treating the lens of a goat placed for 72h in artificial aqueous humor(AAH)of pH 7.8 at room temperature with cataract-causing substance(55 mmol/L of galactose)and in vivo studies were performed on rats via induction with streptozotocin.AST was administered at different dose levels and scrutinize for DC activity.RESULTS:In diabetic rats,AST improved the body weight,blood insulin,and glucose as well as the levels of galactitol in a dose-dependent way,other biochemical parameters i.e.inflammatory mediators and cytokines,and also suppress AR activity.The level of the antioxidant parameters such as superoxide dismutase(SOD),catalase(CAT),and glutathione(GSH)activity were also altered on a diabetic lens after the administration of the AST.CONCLUSION:AST protects against lens opacification to avoid cataracts and polyols formation,indicating that it could be used as a potential therapeutic agent for diabetes.展开更多
[ Objective] The paper was to explore the effect of astragalin on paraoxon-indueed vascular endothelium dysfunction and analyze the potential mecha- nism. [Method]The isolated rat thoracic aorta rings were exposed to ...[ Objective] The paper was to explore the effect of astragalin on paraoxon-indueed vascular endothelium dysfunction and analyze the potential mecha- nism. [Method]The isolated rat thoracic aorta rings were exposed to medium contained paraoxon （3.63 μmol/L）, and astragalin （10 μmol/L） was used to inhib- it the damage effect. Rat thoracic aorta rings were suspended in organ chambers to assess vas orelaxation activity in vitro by acetyleholine （ACh）-induced endotheli- um dependent relaxation reaction （EDRR） and sodium nitroprusside （SNP）-induced endothdium-independent relaxation reaction. [Result]The exposure to parao- xon （3.63 μmol/L） resulted in an inhibition of the EDRR, markedly reduced the level of nitric oxide （NO）, the activity of paraoxonasel （PON1） and superoxide dismutase （SOD）, and significantly increased the level of malondialdehyde （MDA） in isolated rat thoracic aorta. However, the presence of astragalin （10 μmol/L） markedly attenuated the vascular endothelium dysfunction induced by paraoxon via increasing level of NO, activity of PON1 and SOD, as well as reducing level of MDA. In addition, treatment of astragalin （ 10 μmol/L） showed a similar effect to hydrogen peroxide （ 1.0 μmol/L）, a kind of antioxidant, on paraoxon- induced vascular endothelium dysfunction. [ Conclusion] Astragalin could protect the vascular endothelium against the paraoxon-induced dysfunction in isolated rat thoracic aorta, and＇the beneficial effects of astragalin might be concerned with the antioxidation of astragalin due to inhibiting the decreased activity of PONI.展开更多
Objective To investigate the effect of Astragalin on human renal mesangial cells Methods Cultured human mesangial cells were treated with Astragalin and Astragalin serum in different concentrations in the presence ...Objective To investigate the effect of Astragalin on human renal mesangial cells Methods Cultured human mesangial cells were treated with Astragalin and Astragalin serum in different concentrations in the presence or absence of PDGF BB, the proliferation and type Ⅳ collagen secretion of mesangial cells were measured by MTT assay and ELISA, and expression of β1 integrin gene was estimated by reverse transcription polymerase chain reaction (RT PCR) method, sespectively Results After 72 hours Astragalin or Astragalin serum treatment, the proliferation of mesangial cells induced by PDGF BB was inhibited significantly in a dose dependent manner compared with untreated controls ( P <0 05 and P <0 01) After 24 hours of Astragalin or Astragalin serum treatment, the secretion of type Ⅳ collagen protein in presence of PDGF BB was significantly decreased and β1 integrin mRNA level decreased significantly compared with untreated control ( P <0 05, P <0 01) Conclusions Astragalin inhibits cell proliferation and matrix over synthesis which might be mediated, at least, partly by decrease of β1 integrin gene over expression The study suggested that Astragalin might play a role in preventing the progression of chronic renal diseases展开更多
文摘AIM:To investigate the aldose reductase(AR)inhibition capacity of astragalin(AST)against streptozoticin-induced diabetic cataracts(DCs)in rats.METHODS:Ex vivo investigations were conducted by treating the lens of a goat placed for 72h in artificial aqueous humor(AAH)of pH 7.8 at room temperature with cataract-causing substance(55 mmol/L of galactose)and in vivo studies were performed on rats via induction with streptozotocin.AST was administered at different dose levels and scrutinize for DC activity.RESULTS:In diabetic rats,AST improved the body weight,blood insulin,and glucose as well as the levels of galactitol in a dose-dependent way,other biochemical parameters i.e.inflammatory mediators and cytokines,and also suppress AR activity.The level of the antioxidant parameters such as superoxide dismutase(SOD),catalase(CAT),and glutathione(GSH)activity were also altered on a diabetic lens after the administration of the AST.CONCLUSION:AST protects against lens opacification to avoid cataracts and polyols formation,indicating that it could be used as a potential therapeutic agent for diabetes.
基金Supported by Natural Sciences Research Project of Henan Province(No.2010B320011,No.2010B330002)~~
文摘[ Objective] The paper was to explore the effect of astragalin on paraoxon-indueed vascular endothelium dysfunction and analyze the potential mecha- nism. [Method]The isolated rat thoracic aorta rings were exposed to medium contained paraoxon （3.63 μmol/L）, and astragalin （10 μmol/L） was used to inhib- it the damage effect. Rat thoracic aorta rings were suspended in organ chambers to assess vas orelaxation activity in vitro by acetyleholine （ACh）-induced endotheli- um dependent relaxation reaction （EDRR） and sodium nitroprusside （SNP）-induced endothdium-independent relaxation reaction. [Result]The exposure to parao- xon （3.63 μmol/L） resulted in an inhibition of the EDRR, markedly reduced the level of nitric oxide （NO）, the activity of paraoxonasel （PON1） and superoxide dismutase （SOD）, and significantly increased the level of malondialdehyde （MDA） in isolated rat thoracic aorta. However, the presence of astragalin （10 μmol/L） markedly attenuated the vascular endothelium dysfunction induced by paraoxon via increasing level of NO, activity of PON1 and SOD, as well as reducing level of MDA. In addition, treatment of astragalin （ 10 μmol/L） showed a similar effect to hydrogen peroxide （ 1.0 μmol/L）, a kind of antioxidant, on paraoxon- induced vascular endothelium dysfunction. [ Conclusion] Astragalin could protect the vascular endothelium against the paraoxon-induced dysfunction in isolated rat thoracic aorta, and＇the beneficial effects of astragalin might be concerned with the antioxidation of astragalin due to inhibiting the decreased activity of PONI.
文摘Objective To investigate the effect of Astragalin on human renal mesangial cells Methods Cultured human mesangial cells were treated with Astragalin and Astragalin serum in different concentrations in the presence or absence of PDGF BB, the proliferation and type Ⅳ collagen secretion of mesangial cells were measured by MTT assay and ELISA, and expression of β1 integrin gene was estimated by reverse transcription polymerase chain reaction (RT PCR) method, sespectively Results After 72 hours Astragalin or Astragalin serum treatment, the proliferation of mesangial cells induced by PDGF BB was inhibited significantly in a dose dependent manner compared with untreated controls ( P <0 05 and P <0 01) After 24 hours of Astragalin or Astragalin serum treatment, the secretion of type Ⅳ collagen protein in presence of PDGF BB was significantly decreased and β1 integrin mRNA level decreased significantly compared with untreated control ( P <0 05, P <0 01) Conclusions Astragalin inhibits cell proliferation and matrix over synthesis which might be mediated, at least, partly by decrease of β1 integrin gene over expression The study suggested that Astragalin might play a role in preventing the progression of chronic renal diseases
