Antiviral activity of nano-realgar against herpes simplex virus Type II in vitro / 中南大学学报(医学版)

To explore the antiviral activity of nano-realgar against herpes simplex virus Type II (HSV-2) in vitro.
 Methods: Acyclovir (ACV) as a positive control, the cytotoxicity of nano-realgar at different concentrations (including 200.00, 150.00, 100.00, 50.00, 25.00, 12.50, 6.25, 3.13, 1.54, 0.78, 0.39 and 0 mg/L) on normal Vero cells were determined by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. HSV-2 virus titer was determined by plaque assay, and the Vero cells model of HSV-2 infection was established. Subsequently, the antiviral effects of nano-realgar at different concentrations (including 20.00, 10.00, 5.00, 2.50, 1.25, 0.63, 0.31, 0.15, 0.08, 0.04 and 0 mg/L) on infected cells model were evaluated by the observation of cytopathic effect (CPE) and MTT method under the 3 modes including pre-treatment, treatment and direct inactivation.
 Results: The 50% cytotoxic concentration (CC50) of nano-realgar on Vero cells was 37.15 mg/L. The titer of HSV-2 was 7.30 log PFUs/mL. In the 3 modes, the half-maximal effective concentration (EC50) of nano-realgar on HSV-2 infected Vero cells were 0.13, 1.80 and 0.52 mg/L, and the corresponding therapeutic index (TI) were 285.77, 20.64, 71.44, respectively. The TI value of nano-realgar on pre-treatment mode was higher than that of nano-realgar on treatment and direct inactivation modes.
 Conclusion: Nano-realgar can play a good anti-HSV-2 activity in the 3 modes (pre-treatment, treatment and direct inactivation), and the anti-HSV-2 efficacy of nano-realgar on pre-treatment mode is better than that of nano-realagr on other 2 modes.

[A preliminary study on the autophagy level of human periodontal ligament cells regulated by nicotine].

OBJECTIVE: To explore the effect of nicotine on the autophagy level of human periodontal ligament cells (hPDLCs). METHODS: Periodontal tissues collected from premolars for orthodontic treatment reasons were used to culture hPDLCs. Western blot analysis was performed to test the most optimal time and concentration of nicotine on the autophagy level of the hPDLCs. Transmission electron microscope and immunofluorescence observation were carried out to detect the form of autophagosomes and expression of autophagy related protein LC3 in hPDLCs under this optimal condition. RESULTS: Protein expression of LC3Ⅱ was up regulated with the 12 h nicotine stimulating. Besides that, the up regulation of the protein expression of LC3Ⅱ was concentration dependent and nicotine with a concentration of 1×10⁻5 mol·L⁻¹ was the most optimal condition. Transmission electron microscope and immunofluorescence observations indicated that nicotine would activate the autophagy level of hPDLCs by increasing the number of autophagosomes and up regulating the expression of autophagy related protein LC3. CONCLUSIONS: Nicotine could increase autophagy level of hPDLCs, thus affecting the occurrence and development of smoking related periodontitis.

Inhibitory effects of murine angiostatin on implant carcinoma of nude mouse / 中华外科杂志

<p><b>OBJECTIVE</b>To study the effects of murine angiostatin, which was transfected into the human hepatocellular cancer cell line SMMC-7721, on the implant carcinoma of nude mouse.</p><p><b>METHODS</b>The human hepatocellular cancer cell line SMMC-7721, which could express murine angiostatin gene stably, was constructed. The animals were divided into three groups: SMMC-7721 cell was implanted into control group, SMMC-7721/pcDNA3.1 (+) cell was implanted into vector group, and SMMC-7721/pcDNA3.1-mAST cell was implanted into angiostatin group. The carcinoma volume, weight, and microvessel density (MVD) of each group were compared.</p><p><b>RESULTS</b>The implant carcinoma volume in 35 days was (3 538.1 +/- 643.3) mm(3), (3 128.5 +/- 546.6) mm(3), and (755.8 +/- 198.2) mm(3) in the control group, vector group, and angiostatin group. The carcinoma weight of the control group, vector group, and angiostatin group was (6.0 +/- 0.7) g, (5.9 +/- 0.5) g, (2.1 +/- 0.5) g, respectively. The carcinoma MVD was 52.2 +/- 6.6, 49.4 +/- 7.0, and 25.5 +/- 4.1 accordingly. The carcinoma volume, weight, and MVD of the angiostatin group were significantly smaller than those of the control group and vector group (P < 0.01). The inhibitory rate of carcinoma reached 78.6%.</p><p><b>CONCLUSIONS</b>Nude mouse experiments showed that the tumorigenic capacity of cells transfected had been reduced greatly, and that the carcinoma volume, weight and MVD were significantly lower than those of the control group. We conclude that angiostatin inhibits the growth of carcinoma by its inhibition of carcinoma angiogenesis.</p>