We aimed to investigate the effect of etanercept, a tumor necrosis factor-a (TNF-a) inhibitor, on rat cardiomyocyte hypertrophy and its underlying mechanism. Primary neonatal rat cardiomyocytes were isolated from Sprague-Dawley rats. The model of rat cardiomyocyte hypertrophy was induced by endothelin, and then treated with different concentrations of etanercept (1, 10, and 50 mM). After treatment, cell counts, viability and cell apoptosis were evaluated. The mRNA levels of myocardial hypertrophy marker genes, including atrial natriuretic factor (ANF), matrix metalloproteinase (MMP)-9 and MMP-13, were detected by qRT-PCR, and the expressions of apoptosis-related proteins (Bcl-2 and Bax) were measured by western blotting. The protein levels of transforming growth factor-b1 (TGF-b1), interleukin (IL)-1b, IL-6, leukemia inhibitory factor (LIF) and cardiotrophin-1 (CT-1) were determined using enzyme linked immunosorbent assay (ELISA) kits. In the present study, TNF-a level in cardiomyocytes with hypertrophy was significantly enhanced (Po0.05). Compared to the model group, cell number and viability were significantly increased and ratio of apoptotic cells was reduced by etanercept (Po0.05, Po0.01, or Po0.001). In addition, etanercept remarkably reduced the mRNA levels of ANF, MMP-9 and MMP-13, inhibited the expression of Bax, and increased the expression of Bcl-2 compared to the model group (Po0.05). ELISA results further showed that etanercept lowered the levels of IL-1b, IL-6, LIF and CT-1 but not TGF-b1 compared to the model group (Po0.05). Etanercept may protect rat cardiomyocytes from hypertrophy by inhibiting inflammatory cytokines secretion and cell apoptosis.

Sepsis increases the risk of developing liver injury. Previous studies have demonstrated that thymoquinone (TQ) exhibits hepatoprotective properties in vivo as well as in vitro . The present study aimed to investigate the underlying mechanisms of the protective effects of TQ against liver injury in septic BALB/c mice. Male BALB/c mice (age, 8 weeks) were randomly divided into four groups, namely, the control, TQ (50 mg/kg/day) treatment, cecal ligation and puncture (CLP), and TQ + CLP groups. CLP was performed following gavage of TQ for 2 weeks. At 48 h post-CLP, the histopathological alterations in the liver tissue (LT) and plasma levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) were assessed. The present study evaluated microtubule-associated protein light chain 3 (LC3), sequestosome-1 (p62) and beclin 1 protein expression by western blotting and immunostaining , as well as interleukin (IL)-6, IL-1β, IL-10, monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-α (TNF-α) mRNA expression by RT-qPCR. The results of the present study indicated that administration of TQ to mice reduced the histological alterations caused by CLP in LT. TQ inhibited the plasma levels of ALT, AST and ALP in the CLP group. TQ significantly inhibited the elevation of p62, IL-1β, IL-6, MCP-1 and TNF-α levels as well as increased the LC3, beclin 1 and IL-10 levels in LT. PI3K expression in the TQ + CLP group was significantly decreased compared with that in the CLP group. TQ treatment effectively modulated the expression levels of p62, LC3, beclin 1, PI3K and proinflammatory cytokines, and may be an important agent for the treatment of sepsis-induced liver injury.

Salvia miltiorrhiza (SM) is mainly used for the treatment of coronary heart disease in China, but previous studies demonstrated that it also shows anti‑inflammatory effects and the underlying mechanisms of these effects are not well understood. The present study aimed to investigate the effect of an injection of SM powder on the expression of transcription factor Foxp3 (Foxp3) in experimental colitis in mice. Mice were grouped and treated with SM powder for injection at the time of colonic instillation of trinitrobenzene sulfonic acid. Expression studies were performed by quantitative polymerase chain reaction and western blot analysis and histological studies were performed by hematoxylin and eosin staining. Myeloperoxidase activity was also tested for the evaluation of colitis. In the treated groups, the expression of Foxp3 mRNA and protein in the spleen were increased, the inflamed colonic lesions were relieved and the myeloperoxidase activity in the colon decreased significantly. Thus, it was demonstrated that SM exhibited its anti‑inflammatory by promoting Foxp3 expression. SM may be effective for the treatment of inflammatory disease, particularly for inflammatory bowel disease.

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