Quinic acid (QA) and shikimic acid (SA), two kinds of natural organic acids, have been reported to exhibit potent antibacterial activity against Staphylococcus aureus. In this study, the effects of QA and SA on the cellular functions of S. aureus were investigated by measuring the intracellular pH, intracellular and extracellular ATP concentrations, succinate dehydrogenase activity, DNA content, and interactions between SA and QA with S. aureus DNA. Studies of the cellular functions demonstrated that QA could significantly decrease the intracellular pH, whereas SA had no effect on intracellular pH. QA and SA reduced succinate dehydrogenase activity and caused a significant decrease in intracellular ATP concentration but no proportional increase in extracellular ATP. Moreover, QA and SA both could remarkably reduce the DNA content of S. aureus and directly interact with genomic DNA. The results suggested that the effects of QA and SA on cellular functions were distinguishable, although the chemical structures of these two compounds were similar. In conclusion, the results of the present research suggested that SA and QA could be used as antibacterial agents in food preservation.
Structure–activity relationship of 3-p-trans-coumaroyl-2-hydroxyquinic acid, a phenolic compound from needles of Cedrus deodara, against Staphylococcus aureus and its effect on the cellular functions.
The
prevalence of nonalcoholic fatty liver disease (NAFLD), a common
cause of chronic liver disease, continues to increase in parallel
with that of obesity. Currently, there are no preclinical models to
study its complex pathogenesis nor to assess candidate therapies.
We have established a tissue-engineered (TE) liver by seeding cells
into liver-derived matrix scaffolds and then perfusing the scaffolds
with a medium that dynamically provides requisite nutrients, vitamins,
minerals, and hormones. Liver-specific biomatrix scaffolds, comprised
of almost all of the liver’s known extracellular matrix (ECM)
components and matrix-bound soluble signals (e.g., growth factors/cytokines),
were recellularized with human hepatic cell line HepG2 and perfused
with a complete medium enabling the cells to form functioning liver
tissue. By perfusing the system with medium with a high fat content,
the cells established a TE fatty (TEF) liver model paralleling that
of livers in NAFLD patients. The high fat medium containing 500 μM
of free fatty acids (FFAs) (oleic acid:palmitic acid = 2:1) caused
the TEF livers to accumulate 2-times more fat than those in the control
medium over an 8 day culture period and significantly influenced the
capacity of fatty acid synthesis and metabolism. PDK4, CYP2E1, and
CYP7A1 genes associated with NAFLD and other liver diseases were all
up-regulated, and the metabolic activity of CYP3A4 was significantly
impaired. Excess FFAs also induced alterations in transporters and
key enzymes in the lipid biosynthesis pathway. The TEF liver was used
to test if an antisteatotic drug, Metformin, used in patients with
NAFLD, would be able to provide effects paralleling those observed
in some patients. Metformin treatment of the TEF liver model caused
reduced cellular triglycerides, activated AMPK molecule, inhibited
mTORC1 signaling pathway, which thus affected the synthesis and metabolism
of FFAs. Overall, the TEF liver offers a stable and reproducible model
to study the NAFLD development process and antisteatotic drug effects.
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