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This study aimed to examine the anti-inflammatory activity and related mechanisms of alprostadil in lipopolysaccharide (LPS)-treated H9c2 cells.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>Cell morphology was observed under an inverted light microscope, while cell viability was assessed with the 3\u2011(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT) assay. Enzyme-linked immunosorbent assays (ELISA) were conducted to study biochemical indicators of cellular damage, such as released lactate dehydrase (LDH) and troponin, and inflammatory cytokine levels including interleukin-1\u03b2 (IL-1\u03b2), IL-6, IL-17, and tumor necrosis factor-\u03b1 (TNF-\u03b1). The mRNA expression levels of Wnt5a, c\u2011jun N\u2011terminal kinase (JNK), and nuclear factor kappa\u00a0B (NF-\u03baB) were further investigated by real-time quantitative polymerase chain reaction (RT-PCR). The effects of alprostadil on the Wnt5a\/JNK\/NF-\u03baB pathway in H9c2 cells was examined by Western blotting.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>Alprostadil increased the cell viability of LPS-stimulated H9c2 cells, reduced LDH and troponin production, and attenuated IL-1\u03b2, IL-6, IL-17, and TNF-\u03b1 secretion. Moreover, alprostadil reduced the mRNA expression of Wnt5a, JNK, and NF-\u03baB and decreased the expression of Wnt5a, NF-\u03baB, and the ratio of p\u2011JNK\/JNK in H9c2 cells treated with LPS. The siWnt5a or JNK inhibitor SP600125 significantly augmented the inhibitory effects of alprostadil on the Wnt5a\/JNK\/NF-\u03baB pathway.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusion<\/jats:title>\n                <jats:p>Our results show that alprostadil has anti-inflammatory effects and could attenuate LPS-induced injury in H9c2 cardiomyocytes via the Wnt5a\/JNK\/NF-\u03baB pathway.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1007\/s00059-019-4837-0","type":"journal-article","created":{"date-parts":[[2019,7,16]],"date-time":"2019-07-16T12:12:54Z","timestamp":1563279174000},"page":"130-138","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Alprostadil attenuates LPS-induced cardiomyocyte injury by inhibiting the Wnt5a\/JNK\/NF-\u03baB pathway","Alprostadil schw\u00e4cht LPS-induzierte Kardiomyozytensch\u00e4digung durch Hemmung des Wnt5a\/JNK\/NF-\u03baB-Signalwegs ab"],"prefix":"10.1007","volume":"45","author":[{"given":"T.","family":"Yu","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D.","family":"Dong","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.","family":"Guan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J.","family":"Sun","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M.","family":"Guo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Q.","family":"Wang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2019,7,16]]},"reference":[{"issue":"1","key":"4837_CR1","doi-asserted-by":"publisher","first-page":"112","DOI":"10.1186\/s13054-018-2043-8","volume":"22","author":"RR Ehrman","year":"2018","unstructured":"Ehrman\u00a0RR, Sullivan\u00a0AN, Favot\u00a0MJ et\u00a0al (2018) Pathophysiology, echocardiographic evaluation, biomarker findings, and prognostic implications of septic cardiomyopathy: A\u00a0review of the literature. 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