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Methicillin-resistant Staphylococcus aureus (MRSA) is a serious threat to global public health due to its capacity of tolerate conventional antibiotics. Medicinal plants are traditionally used to treat infectious diseases caused by bacterial pathogens. In the present study, 16 medicinal plants were screened for antibacterial activities to preselect more effective species. Ethanol extracts of selected medicinal plants (Caesalpinia sappan L., Glycyrrhiza uralensis Fisch., Sanguisorba officinalis L., and Uncaria gambir Roxb) were partitioned successively with different solvents (n-hexane, chloroform, ethyl acetate, 1-butanol, and water). Disc diffusion assay and broth microdilution were performed to evaluate the antibacterial activities of plant extracts and fractions against Staphylococcus aureus strains. Furthermore, the cytotoxicity of the extracts and fractions was determined against the human hepatoma (HepG2) and human lung carcinoma (A549) cell lines using a trypan blue exclusion method. A few extracts and fractions showed significant inhibitory effects on the bacterial growth of all tested strains, including multidrug-resistance (MDR) clinical isolates. The ethyl acetate fraction of C. sappan had the most potent effects with minimum inhibitory/bactericidal concentrations (MIC/MBC) of 31.2/62.5 μg/mL and showed low cytotoxicity with over 90% cell viability in both cells. Our results suggest that medicinal plants have considerable potential as alternatives to conventional antibiotics.

Drug-induced liver injury (Dili) is the most common adverse event causing drug disapprovals and withdrawals. roughly 10% of drug-induced hepatotoxicity is non-steroidal anti-inflammatory drug (NSAID)-related. To find NSAID-induced hepatotoxic markers, we analyzed gene and protein expression levels using human primary hepatocytes treated with 6 nSaiDs. To examine cellular responses to drug treatments, we conducted cell viability assay. Hepatocytes treated with diclofenac and sulindac showed significantly lower cell viability than those treated by other drugs. From the PCr data, a total of 29 genes were significantly modulated by diclofenac and sulindac. In addition, we treated human primary hepatocytes with representative non-nSaiD hepatotoxic drugs such as acetaminophen, valporic acid, and flutamide and performed real-time PCR to select NSAID-specific hepatotoxic markers. The expressions of 4 genes (ABCB1, LPL, HYOU1, GADD45A) and 3 proteins (lPl, HYOU1, GADD45A) showed significant modulation. our findings may provide molecular mechanisms involved in nSaiD-induced hepatotoxicity.

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