Shenfuqiangxin Capsule inhibits apoptosis through mitogen-activated protein kinase signal pathway in rats with cardio-renal syndrome induced by infrarenal aortic-clamping

OBJECTIVE： To investigate the effect of Shenfuq- iangxin capsule and the underlying mechanism on cardio-renal syndrome （CRS） in rats induced by infrarenal aortic-clamping after renal ischaemia. METHODS： Male Wistar rats underwent infrarenal aortic-clamping after renal ischaemia or sham operation. Th...

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Bibliographic Details
Published inJournal of traditional Chinese medicine Vol. 37; no. 1; pp. 80 - 87
Main Author Wang Lei Wang Zi Yuan Ling Hao Di Lu Nan Li Xu
Format Journal Article
LanguageEnglish
Published China 01.02.2017
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Summary:OBJECTIVE： To investigate the effect of Shenfuq- iangxin capsule and the underlying mechanism on cardio-renal syndrome （CRS） in rats induced by infrarenal aortic-clamping after renal ischaemia. METHODS： Male Wistar rats underwent infrarenal aortic-clamping after renal ischaemia or sham operation. The surviving CRS rats were divided randomly into three groups： CRS group （CRS ＋ 10 mL. kg^-1·d^-1 pure water by gavage）, SFQX group （CRS ＋ 13.2 g crude drug·kg^-1·d^- 1 Shenfuqiangxin by gavage）, and handle region peptide（HRP） group（CRS＋10 mgl kg HRP by vein）. Sham operation rats were given 10 mL·kg^-1·d^-1 pure water. Treatments were given 8 weeks after surgery, which lasted for 4 weeks. The rats were detected for heart structure and function by transthoracic echocardiography. PPR mRNA was detected by Reverse Transcription Polymerase Chain Reaction （RT-PCR）. To determine whether the mitogen-activated protein kinase （MAPK） signal pathway is included in the heart and kidney protective function of Shenfuqiangxin capsule, MAPK related proteins such as posophorylated C-Jun amino terminal kinase （p-JNK）, posophorylated extracellular signal-regulated kinase 1/2 （p-ERK1/2）, posophor- ylated p38 （p-p38） were examined by Western BLot. Apoptosis in heart and kidney tissues were detected by dUTP Nick End Labeling staining. RESULTS： Shenfuqiangxin capsule alleviated myo- cardial apoptosis and inhibited PRR mRNA expres- sion and p-JNK, p-ERK1/2, p-p38 proteins expres- sion in CRS rats. CONCLUSION： All the results suggest that Shenfuq- iangxin capsule improves the injured heart and kid- ney function maybe through inhibition of MAPK response pathway.
Bibliography:Renal ischaemia; Cardi-orenal syndrome; Shenfuqiangxin capsule; Mitogen-activatedprotein kinases; Infrarenal aortic-clamping; （Pro）rennin receptor
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OBJECTIVE： To investigate the effect of Shenfuq- iangxin capsule and the underlying mechanism on cardio-renal syndrome （CRS） in rats induced by infrarenal aortic-clamping after renal ischaemia. METHODS： Male Wistar rats underwent infrarenal aortic-clamping after renal ischaemia or sham operation. The surviving CRS rats were divided randomly into three groups： CRS group （CRS ＋ 10 mL. kg^-1·d^-1 pure water by gavage）, SFQX group （CRS ＋ 13.2 g crude drug·kg^-1·d^- 1 Shenfuqiangxin by gavage）, and handle region peptide（HRP） group（CRS＋10 mgl kg HRP by vein）. Sham operation rats were given 10 mL·kg^-1·d^-1 pure water. Treatments were given 8 weeks after surgery, which lasted for 4 weeks. The rats were detected for heart structure and function by transthoracic echocardiography. PPR mRNA was detected by Reverse Transcription Polymerase Chain Reaction （RT-PCR）. To determine whether the mitogen-activated protein kinase （MAPK） signal pathway is included in the heart and kidney protective function of Shenfuqiangxin capsule, MAPK related proteins such as posophorylated C-Jun amino terminal kinase （p-JNK）, posophorylated extracellular signal-regulated kinase 1/2 （p-ERK1/2）, posophor- ylated p38 （p-p38） were examined by Western BLot. Apoptosis in heart and kidney tissues were detected by dUTP Nick End Labeling staining. RESULTS： Shenfuqiangxin capsule alleviated myo- cardial apoptosis and inhibited PRR mRNA expres- sion and p-JNK, p-ERK1/2, p-p38 proteins expres- sion in CRS rats. CONCLUSION： All the results suggest that Shenfuq- iangxin capsule improves the injured heart and kid- ney function maybe through inhibition of MAPK response pathway.
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ISSN:0255-2922