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BMC Complementary and Alternative Medicine 2014-May

Effects of astragalus injection on the TGFβ/Smad pathway in the kidney in type 2 diabetic mice.

Vain rekisteröityneet käyttäjät voivat kääntää artikkeleita
Kirjaudu sisään Rekisteröidy
Linkki tallennetaan leikepöydälle
Yanna Nie
Shuyu Li
Yuee Yi
Weilian Su
Xinlou Chai
Dexian Jia
Qian Wang

Avainsanat

Abstrakti

BACKGROUND

In traditional Chinese medicine, astragalus injection is used to treat diabetic nephropathy (DN). The current study was conducted to determine the effects of astragalus injection on DN by assessing potential modulation of the transforming growth factor beta TGFβ/Smad signaling pathway.

METHODS

Diabetic, male KKAy mice, aged 14 weeks were randomly divided into a model group and an astragalus treatment group, while age-matched male C57BL/6J mice were selected as controls. The treatment group received daily intraperitoneal injections of astragalus (0.03 ml/10 g.d), while the model group received injections of an equivalent volume of saline. Mice were euthanized after 24 weeks. Serum samples were obtained from animals in each group, and blood glucose, creatinine, and urea nitrogen levels were measured. Tissue samples from the kidney were used for morphometric studies. The expression of TGFβ1, TGFβR-Ι, Smad3, and Smad7 were evaluated using reverse transcription-polymerase chain reaction (RT-PCR), and western blot analysis.

RESULTS

Mice in the model group became obese, and suffered complications, including hyperglycemia, polyuria, and proteinuria. Astragalus treatment significantly reduced albuminuria, improved renal function, and ameliorated changes in renal histopathology. Moreover, administration of astragalus injection increased Smad7 expression, and inhibited the expression of TGFβR-Ι, Smad3 and its phosphorylation, and decreased the mRNA level of TGFβ1.

CONCLUSIONS

The TGFβ/Smad signaling pathway plays an important role in the development of DN. Administration of astragalus injection could prevent or mitigate DN by rebalancing TGFβ/Smad signaling, and could play a protective role in DN-induced renal damage in KKAy mice.

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