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Abstract Title:

Astragaloside-IV prevents acute kidney injury and inflammation by normalizing muscular mitochondrial function associated with a nitric oxide protective mechanism in crush syndrome rats.

Abstract Source:

Ann Intensive Care. 2017 Sep 4 ;7(1):90. Epub 2017 Sep 4. PMID: 28871521

Abstract Author(s):

Isamu Murata, Yuji Abe, Yuka Yaginuma, Kayako Yodo, Yuka Kamakari, Yurika Miyazaki, Daichi Baba, Yuko Shinoda, Toru Iwasaki, Kunihiko Takahashi, Jun Kobayashi, Yutaka Inoue, Ikuo Kanamoto

Article Affiliation:

Isamu Murata

Abstract:

BACKGROUND: Crush syndrome (CS) is a serious medical condition characterized by muscle cell damage resulting from decompression after compression (i.e., ischemia/reperfusion injury). A large number of CS patients develop cardiac failure, kidney dysfunction, and systemic inflammation, even when fluid therapy is administered. We evaluated whether the administration of astragaloside-IV (AS)-containing fluid improved survival by preventing kidney and muscular mitochondrial dysfunction in a rat model of CS.

RESULTS: The CS model was generated by subjecting anesthetized rats to bilateral hind limb compression with a rubber tourniquet for 5 h. Rats were then randomly divided into four groups: (1) sham; (2) CS with no treatment; (3) CS with normal saline treatment; and (4) CS with normal saline + 10 mg/kg AS. AS-containing fluid improved kidney function by improving shock and metabolic acidosis in CS rats. In addition, there was areduction in oxidative damage. The attenuation of hyperkalemia was significantly related to improving muscle injury via preventing mitochondrial dysfunction. Moreover, this mitochondria protection mechanism was related to the nitric oxide (NO) generated by activation of endothelial nitric oxide synthase, which provided an anti-oxidative and anti-inflammatory effect.

CONCLUSIONS: Treatment with AS-containing fluid led to a dramatic improvement in survival following CS because of direct and indirect anti-oxidative effects in the kidney, and improvements in mitochondrial dysfunction and inflammation owing to AS acting as an NO donor in injured muscle.

Study Type : Animal Study

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Sayer Ji
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