[Essential oil from Artemisia lavandulaefolia induces apoptosis and necrosis of HeLa cells].

OBJECTIVE: To investigate the effects of Artemisia lavandulaefolia essential oil on apoptosis and necrosis of HeLa cells. METHODS: Cell viability was assayed using MTT method. The morphological and structure alterations in HeLa cells were observed by microscopy. Furthermore, cell apoptosis was measured by DNA Ladder and flow cytometry. DNA damage was measured by comet assay, and the protein expression was examined by Western blot analysis. RESULTS: MTT assay displayed essential oil from Artemisia lavandulaefolia could inhibit the proliferation of HeLa cells in a dose-dependent manner. After treated with essential oil of Artemisia lavadulaefolia for 24 h, HeLa cells in 100 and 200 microg/mL experiment groups exhibited the typical morphology changes of undergoing apoptosis, such as cell shrinkage and nucleus chromatin condensed. However, the cells in the 400 microg/mL group showed the necrotic morphology changes including cytomembrane rupture and cytoplasm spillover. In addition, DNA Ladder could be demonstrated by DNA electrophoresis in each experiment group. Apoptosis peak was also evident in flow cytometry in each experiment group. After treating the HeLa cells with essential oil of Artemisia lavadulaefolia for 6 h, comet tail was detected by comet assay. Moreover, western blotting analysis showed that caspase-3 was activated and the cleavage of PARP was inactivated. CONCLUSION: Essential oil from Artemisia lavadulaefolia can inhibit the proliferation of HeLa cells in vitro. Low concentration of essential oil from Artemisia lavadulaefolia can induce apoptosis, whereas high concentration of the compounds result in necrosis of HeLa cells. And,the mechanism may be related to the caspase-3-mediated-PARP apoptotic signal pathway.

Dietary restriction reduces blood lipids and ameliorates liver function of mice with hyperlipidemia.

Dietary restriction (DR) can delay senescence, prolong lifespan of mammals and improve their learning-memory activity. The purpose of the study was to explore the effects of DR on hypolipidemic action and liver function of mice with hyperlipidemia. To investigate these effects, hyperlipidemia mouse models were established with high-fat diet (HFD) (34% of energy), then randomly divided into HFD group, DR30% group and DR50% group. Mice in DR30% and DR50% group were respectively supplied with HFD as much as about 70% and 50% of the consumption of HFD in the mice of HFD group. Rats in control group were fed routinely. After DR for 5 weeks, the average body weight, liver weight, liver index, serum lipids and glucose levels in both DR groups decreased significantly as compared with the HFD group (P<0.05 or P<0.01), so did alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH) levels and the ratio of LDL-C/HDL-C in the DR50% group (P<0.05 or P<0.01). Histopathology examination of liver tissues further proved ameliorative effect of DR on liver function. Western blotting showed that DR significantly increased the expression of silent mating type information regulation 2 homolog 1 (SIRT1) in liver and adipose, while notably decreased the expression of peroxisome proliferators-activated receptors-gamma (PPARγ) in adipose (P<0.05 or P<0.01). The increase of SIRT1 and decrease of PPARγ may be a mechanism by which DR reduces blood lipids and ameliorates liver function.

Gynura procumbens ethanolic extract suppresses osteosarcoma cell proliferation and metastasis in vitro.

Gynura procumbens is a traditional herb used for the treatment of inflammation, rheumatism and viral infections, although the antitumor effect and its potential mechanisms of action remain unclear. In the present study, the antitumor effect of Gynura procumbens ethanolic extract (GPE) on the osteosarcoma (OS) cell line, U2-OS, was investigated in vitro. Cell proliferation and apoptosis were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry assays, respectively. Transwell invasion and wound healing assays were performed to investigate the invasion and migration of the U2-OS cells. The results showed that GPE was able to inhibit U2-OS cell proliferation and metastasis and induce cell apoptosis. Furthermore, the expression of the NF-κBp65 protein was detected by western blotting to evaluate the effects of GPE on the nuclear transfer of NF-κB. It was demonstrated that the expression of the NF-κBp65 protein was significantly decreased by GPE. This indicated that GPE was able to inhibit the nuclear transfer of NF-κB. The study shows that GPE is able to induce apoptosis and suppress proliferation and metastasis in U2-OS cells via the inhibition of the nuclear translocation of NF-κB.