This study was conducted to assess the protective effects of the aqueous green tea extract (GTE) against particulate matter (PM)2.5-induced cardiac dysfunction in BALB/c mice. The administration of GTE increased the body weight change and reduced the heart index. GTE suppressed the increase in creatine kinase MB isoenzyme (CKMB) and lactate dehydrogenase (LDH) contents in mice serum. GTE protected the antioxidant system damage by regulating the superoxide dismutase (SOD) activity, reduced glutathione (GSH) contents, and malondialdehyde (MDA) contents in heart tissues. In addition, GTE down regulated the inflammatory reaction by inhibiting the protein expression levels of Toll-like receptor (TLR)2, TLR4, phosphoylated nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha (p-IκB-α), caspase-1 (Cas-1), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), tumor necrosis factor-a (TNF-α), and internluekin-1beta (IL-1β). The consumption of GTE suppressed the cardiac cytotoxicity by regulating the protein expression levels of phosphorylated protein kinase B (p-Akt), phosphorylated c-Jun N-terminal kinase (p-JNK), heme oxygenase-1 (HO-1), B-cell lymphoma 2 (BCl-2), and BCl-2 associated X (BAX). This study suggests that GTE might be a potential material to protect PM2.5-induced cardiac damage and inflammation via the TLR pathway.