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This study aimed to explore the role of MALAT1 in sepsis-induced cardiac inflammation and dysfunction. We constructed the rat sepsis models through cecal ligation and puncture (CLP). The cardiac function, including left ventricular peak pressure (LVPP), left ventricular end diastolic pressure (LVEDP) and maximum rate of rise/fall of left ventricle pressure (± dp/dtmax) as well as the contents of serum cardiac troponin I (CTn-I), creatine kinase (CK), and creative kinase isoenzyme MB (CK-MB) were detected after modeling. Additionally, the blood cytokines levels including tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), IL-1β, IL-10, IL-17, and IFN-γ and complement proteins of C5 and C5a after modeling were detected. Moreover, luciferase reporter assay was performed to investigate the regulatory miRNA of MALAT1. The protein expressions of p38 MAPK, NFκB, JAK2 and STAT3 were detected using western blot. MALAT1 expression was significantly upregulated in CLP-induced sepsis model. MALAT1 knockdown significantly increased LVSP and + dp/dsmax, decreased LVEDP and − dp/dsmax of sepsis as well as levels of cTn-I, CK, CK-MB, TNF-α, IL-1β, IL-6, IL-10, IL-17, IFN-γ, C5 and C5a. MALAT1 was regulated by miR-125b, and miR-125b overexpression and MALAT1 knockdown had similar effects on sepsis rat models. Furthermore, MALAT1 induced cardiac dysfunction and inflammation in CLP models via activating p38 MAPK/NFκB. Our results suggest that MALAT1 aggravates cardiac inflammation and dysfunction in sepsis, which is achieved via interaction with miR-125b and p38 MAPK/NFκB. MALAT1 may serve as a diagnostic marker and therapeutic target in sepsis.MALAT1 expression was significantly upregulated in CLP-induced sepsis model.MALAT1 regulated sepsis-induced cardiac inflammation and dysfunction in model rats.miR-125b overexpression and MALAT1 knockdown had similar effect on sepsis rats.MALAT1 induced cardiac dysfunction and inflammation in model rats via p38 MAPK/NFκB.