ABSTRACT
We investigate the role and mechanism of imbalance via Th9 cells and Th17/Treg cells in the inflammatory and fibrotic phases of pulmonary fibrosis in mice. A total of mice were split into normal saline (control group) and inflammation and fibrosis mouse models (study group) randomly, and lung tissues and bronchoalveolar lavage fluid (BALF) were obtained from mice at the inflammatory and fibrotic phases on the 7th and 28th day, respectively. The degenerative changes in the mouse lung tissue were then visible using H&E staining. The expression of CCR6 and IL-9 in the lung tissues of two groups was examined through an immunohistochemistry assay. Fluorescence PCR was used to assess the expression of PU.1 mRNA in BALF, and flow cytometry was performed to identify the expression of Th17 and Treg. (1). The level of pulmonary fibrosis and lung inflammation in the research group was significantly higher than in the control group. (2). The expression of Th17, CCR6, IL-9 and PU.1 mRNA was substantially higher (P<0.05) in the research group at different time points; the expression level of Treg cells was considerably lower (P<0.05) in the research group than in the control group. (3). CCR6, IL-9 and PU.1 mRNA levels were statistically directly associated (P<0.05) with Th17 and inversely correlated 40 with Regulatory T cells (Tregs). CCR6 and Th9 cells may be involved in 45 developing Th17/Treg imbalance in the immune inflammation of pulmonary fibrosis, which promotes fibrocyte proliferation in lung tissue.
ABSTRACT
Resveratrol is a natural compound present in red grapes and red wine, and is often consumed in the human diet. The chemopreventive and chemotherapeutic potential of resveratrol in hepatocellular carcinoma (HCC), one of the most common types of liver cancer, has received much attention in recent years. However, the side-effects of resveratrol stimulation are of concern due to the high doses administered to humans. This study investigated the effects of resveratrol on the mRNA expression of pten and bcl-xl in HepG2 cells using semi-quantitative and quantitative PCR. This study demonstrated that 200 µmol/l resveratrol stimulation for 12 h resulted in the inhibition of HepG2 proliferation, reduced pten and increased bcl-xl mRNA expression. The data suggest that (a) the anticancer mechanism of resveratrol does not involve the induction of pten and inhibition of bcl-xl expression and (b) resveratrol induces a cellular self-protection response, which underlies the cellular chemoresistance against resveratrol in HepG2 cells.
