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https://www.selleckchem.com/products/U0126.html The expression of miR‑142‑3p was significantly increased while AC9 and cAMP expression significantly decreased in CCI rats. However, AC9 overexpression significantly increased the levels of cAMP protein. Luciferase reporter assay also proved that AC9 is the target gene of miR‑142‑3p. Moreover, miR‑142‑3p silencing was found to reduce neuropathic pain in CCI rats by upregulating the expression of AC9. It was also found that cAMP activation can relieve neuropathic pain and promote the expression of AMPK‑related proteins in CCI rats. Silencing miR‑142‑3p can target AC9 to reduce the expression of inflammatory factors and neuropathic pain in CCI rats by increasing the expression of cAMP/AMPK pathway‑related proteins.Bone marrow mesenchymal stem cells (BMSCs) are accepted as a form of cellular therapy to improve cardiac function following acute myocardial infarction (AMI). The present study was performed to investigate the synergistic effect of ultrasound‑targeted microbubble destruction (UTMD)‑mediated Galectin‑7‑small interfering (si)RNA with the homing of BMSCs for AMI. The rat model of AMI was established, followed by identification of BMSCs. Rats with AMI received BMSC transplantation, BMSC transplantation + UTMD + siRNA negative control, or BMSC transplantation + UTMD + Galectin‑7‑siRNA. The cardiac function, hemodynamics indexes, degree of myocardial fiber injury and expression of apoptosis‑related proteins in myocardial tissues of rats were detected. The homing of BMSCs was observed, and the indexes of myocardial microenvironment and the TGF‑β/Smads pathway‑related proteins in myocardial tissues were determined. AMI rats treated with UTMD‑mediated Galectin‑7‑siRNA exhibited improved cardiac function and hemodynamics‑related indices, decreased myocardial fiber injury and apoptotic cells, as well as enhanced homing ability of BMSCs, improved myocardial microenvironment, and suppressed TGF‑β1/Smads pathway activation.

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