Resveratrol protects against atherosclerosis by downregulating the PI3K/AKT/mTOR signaling pathway in atherosclerosis model mice.

Atherosclerosis is a cardiovascular disease, which is characterized by the interaction between carbohydrates, lipids, cells and various other molecules and genetic factors. Previous studies have demonstrated that resveratrol (RV) served protective roles in numerous types of human disease by regulating different signaling pathways. The aim of the present study was to investigate the therapeutic effects of RV and analyze the potential RV-mediated mechanism in umbilical vein endothelial cells (UVECS) in atherosclerosis model mice. Reverse transcription-quantitative PCR, western blotting and immunohistochemistry were used to analyze the therapeutic effects of RV both in vitro and in vivo. The results demonstrated that total cholesterol, triglycerides, low-density lipoprotein cholesterin and high-density lipoprotein cholesterin levels were significantly decreased in the RV group compared with the control group. RV demonstrated significant anti-atherosclerotic activity, which was determined through the atherogenic index, 3-hydroxy-3-methyl-glutaryl-Coa (HMG-CoA) reductase activity and marker enzymes, such as lactate dehydrogenase, creatine phosphokinase, aspartate transaminase, alanine transaminase and alkaline phosphatase. It was also observed that RV treatment significantly decreased the area of the arteriosclerotic lesion in the RV group compared with the control, as well as significantly decreasing the expression levels of matrix metalloproteinase-9 and CD40 ligand (CD40L) in arterial lesion tissue compared with the control group. Serum expression levels of tumor necrosis factor-α and C-reactive protein were also significantly decreased by RV treatment compared with the control group. Furthermore, RV treatment significantly decreased the expression levels of PI3K, AKT and mTOR in UVECS in vitro. In conclusion, these results suggested that the anti-atherosclerotic activity of RV may be due to its modulatory activity over the PI3K/AKT/mTOR signaling pathway. These findings suggested a potential novel treatment option for patients with atherosclerosis.

Assessment of Meibomian Gland (MD) Impairment Among Seasonal Allergic Conjunctivitis (SAC) Patients.

BACKGROUND Allergic conjunctivitis, one of the frequently occurring ocular surface diseases, can cause mucus discharge, itchy sensation, conjunctival hyperemia, and papillary formation. Seasonal allergic conjunctivitis (SAC) is associated with xerophthalmia and instability of tear film. Meibomian gland (MG) can secrete lipids to avoid xerophthalmia. However, there have been few reports on MG morphological alterations of SAC patients. This study aimed to examine the morphological alterations of MG among SAC patients. MATERIAL AND METHODS Our study included 89 eyes from 89 patients with SAC and 112 eyes of healthy volunteers. The symptoms were assessed by ocular surface disease index (OSDI) questionnaire. Then, the tests shown below were carried out, including tear evaporation rate from the ocular surface (TEROS), slit-lamp examination, break-up time (BUT) of tear film, Schirmer test I, vital staining, meibography, and meibum expression grading. MG was examined with laser scanning confocal microscopy (LSCM). RESULTS Relative to the control group, the OSDI was significantly higher in the SAC group. TEROS values, BUT, vital staining, MG expression, MG distortion rates, and MG dropout grades were significantly worse in the SAC group compared with the control group. As suggested by LSCM, SAC patients had markedly worse averages of parameters compared with controls. CONCLUSIONS The patients with SAC have more significant morphological and cytological changes in the MG. The Keratograph 5M system and LSCM are effective methods for evaluating MG status and ocular surface diseases.

Curcumin Inhibits Proliferation of Epstein-Barr Virus-Associated Human Nasopharyngeal Carcinoma Cells by Inhibiting EBV Nuclear Antigen 1 Expression.

This investigation aims to study the effect of curcumin on the proliferation, cycle arrest, and apoptosis of Epstein-Barr virus- (EBV-) positive nasopharyngeal carcinoma (NPC) cells. EBV+ NPC cells were subjected to curcumin treatment. The cell viability was evaluated with the CCK-8. Cell cycle and apoptosis were analyzed by flow cytometry analysis. Expression (protein and mRNA) levels were detected with western blotting and quantitative real-time PCR, respectively. Curcumin efficiently reduced the viability of EBV+ NPC cells. Curcumin induced the cycle arrest of the HONE1 and HK1-EBV cells positive for EBV. Moreover, curcumin treatment promoted the NPC cell apoptosis, via the mitochondria- and death receptor-mediated pathways. Furthermore, curcumin decreased the expression of EBNA1 in the HONE1 and HK1-EBV cells and inhibited the transcriptional level of EBNA1 in the HeLa cells. Curcumin induced EBNA1 degradation via the proteasome-ubiquitin pathway. In addition, curcumin inhibited the proliferation of HONE1 and HK1-EBV cells positive for EBV, probably by decreasing the expression level of EBNA1. In both the HONE1 and HK1-EBV cells, curcumin inhibited the EBV latent and lytic replication. Curcumin could reduce the EBNA1 expression and exert antitumor effects against NPC in vitro.