Figure 7.

Overexpression of miR-410-3p Represses LPS-Induced Mitochondrial Dysfunction and Chemokine Production in Cardiomyocytes by Regulating TLR2 In Vitro

(A) Detection of miR-410-3p and TLR2 expression patterns by qRT-PCR in LPS-exposed cardiomyocytes treated with sh-TLR2, miR-410-3p agomir, or both miR-410-3p agomir and TLR2, normalized to U6 and β-actin, respectively. (B) Measurement of the swelling degree of myocardial mitochondria. (C) Measurement of mitochondrial ATP levels in the supernatant in LPS-exposed cardiomyocytes treated with sh-TLR2, miR-410-3p agomir, or both miR-410-3p agomir and TLR2. (D) Detection of MMP by JC-1 assay in LPS-exposed cardiomyocytes treated with sh-TLR2, miR-410-3p agomir, or both miR-410-3p agomir and TLR2, normalized to LPS-exposed cardiomyocytes treated with sh-NC. (E–H) Determination of serum CXCL1 (E), CXCL9 (F), CCL5 (G), and CCL7 (H) levels by ELISA in LPS-exposed cardiomyocytes treated with sh-TLR2, miR-410-3p agomir, or both miR-410-3p agomir and TLR2; ∗p < 0.05 versus the LPS + agomir-NC group (cardiomyocytes transduced with agomir-NC and treated with LPS); #p < 0.05 versus the LPS + miR-410-3p agomir group (cardiomyocytes transduced with miR-410-3p agomir and treated with LPS). Measurement data were expressed as mean ± standard deviation. Comparison between two groups was conducted by unpaired t test. Cell experiments were repeated independently three times.