Heilaohuacid G, a new triterpenoid from Kadsura coccinea inhibits proliferation, induces apoptosis, and ameliorates inflammation in RA-FLS and RAW 264.7 cells via suppressing NF-𝜠B pathway.

Heilaohu, the roots of Kadsura coccinea, has been used in Tujia ethnomedicine to treat rheumatic arthritis (RA). Heilaohuacid G (1), a new 3,4-seco-lanostane type triterpenoid isolated from the ethanol extract of Heilaohu, whose structure was determined using HR-ESI-MS data, NMR spectroscopic analyses, and ECD calculations. In this study, our purpose is to elucidate the mechanisms of Heilaohuacid G in the treatment of RA by inhibited proliferation of rheumatoid arthritis-fibroblastoid synovial (RA-FLS) cells and inhibited the inflammatory reactions in LPS-induced RA-FLS and RAW 264.7 cell lines via inhibiting NF-κB pathway. The biological activity screening experiments indicated that Heilaohuacid G significantly inhibited proliferation of RA-FLS cells with IC50 value of 8.16 ± 0.47 µM. CCK-8 assay, ELISA, flow cytometry assay, and Western blot were used to measure the changes of cell viability, apoptosis, and the release of inflammatory cytokines. Heilaohuacid G was found not only induced RA-FLS cell apoptosis, but also inhibited the inflammatory reactions in LPS-induced RA-FLS and RAW 264.7 cell lines via inhibiting NF-κB pathway. Furthermore, Heilaohuacid G (p.o.) at doses of 3.0, 6.0, and 12.0 mg/kg and the ethanol extracts of Heilaohu (p.o.) at doses of 200, 400, and 800 mg/kg both were confirmed antiinflammatory effects on xylene-induced ear mice edema model.

Native musk and synthetic musk ketone strongly induced the growth repression and the apoptosis of cancer cells.

BACKGROUND: Musk is widely used in clinical practice for its anti-cancer properties. Here, we treated various types of cancer using musk to determine which cancers are sensitive to musk treatment. We also compared effects of native musk and synthetic musk ketone in cancer cells. Furthermore, we investigated mechanisms underlying effects of musk. METHODS: Twenty two cancer cell lines were treated with musk. Cell proliferation and apoptosis analyses were carried out. Native musk and synthetic musk ketone were analyzed by gas chromatograph-mass spectrometer (GC-MS) assay. Differentially expressed genes were determined by microarray and quantitative real-time polymerase chain reaction. RESULTS: Native musk strongly induced the growth repression and the apoptosis in the majority of cancer cell lines in a dose-dependent manner, but distinct types of cancer showed significantly different reactions. Cancer cells which originated from epithelial cells showed higher sensitivity for musk treatment. By contrast, leukaemia and lymphoma cells were not sensitive. GC-MS analysis demonstrated that native musk contains more than 30 contents in which musk ketone is a major component; synthetic musk ketone was consistent with natural musk ketone, and the used sample of synthetic musk ketone contained only sole component. Similar to native musk, synthetic musk ketone induced the growth repression and the apoptosis of cancer cells. Additionally, numerous genes were differentially expressed in lung cancer cells after native musk treatment. These differentially expressed genes were involved in many signalling pathways. Among these pathways, apoptosis-related pathways included interleukin family, tumor necrosis factor family, and MAPK signalling pathway. Native musk and synthetic musk ketone can up-regulate IL-24 (interleukin family) and DDIT3 (MAPK signalling pathway) in lung cancer cells. CONCLUSIONS: This research provided strong evidence that native musk and synthetic musk ketone can induce the growth repression and the apoptosis of cancer cells. However, the selection of sensitive cancer patient for individualized treatment is a key step in clinical application. Synthetic musk ketone can substitute for native musk to treat cancer patients. Musk might induce the growth repression and the apoptosis of lung cancer cells through up-regulating IL-24 and DDIT3 expressions.

Antimicrobial efficacy of chloroxylenol and chlorhexidine in the treatment of infected root canals.

PURPOSE: To investigate the antimicrobial efficacy of a chlorhexidine gluconate (2.0%) and of an ethanolic chloroxylenol solution (10%) as a temporary root canal dressing against selected test microorganisms (Staphylococcus aureus, Streptococcus faecium, Escherichia coli, Candida albicans). MATERIALS AND METHODS: Extracted single-rooted human teeth were instrumented up to size 40. After removal of the smear layer suspensions of the test microorganisms were inserted into the root canals. After incubation for 48 hrs each suspension of the test organisms was removed and the root canals were filled with one of the two different disinfectants. The teeth were then incubated for 48 hrs. Twelve teeth and three controls were used for each of the four test organisms and each of the two regimens. After incubation, each root canal was instrumented and the removed canal wall dentin was examined microbiologically. RESULTS: With a contact time of 48 hrs between the two disinfectants and the four bacterial suspensions the medications led to a total killing of microorganisms in 82% of a total of 96 contaminated teeth. In the dentin layer situated 50 microm from the root canal, both medications achieved bacterial killing in a range from 99.9% to 99.99%, depending on the test organism. There were no significant differences (P> 0.1) between the relative antimicrobial activity of the two root canal dressings.

[The results of an experimental study of an anti-Opisthorchis preparation made from plant raw material]. / Rezul'taty éksperimental'nogo izucheniia protivoopistorkhoznogo preparata iz rastitel'nogo syr'ia.

Agents and biologically active fractions derived from medical plants grown in Siberia were tested in vitro and in vivo. The extract from the aspen bark displayed the highest antiopisthorchiatic activity. This agent given at a concentration of 10(-3) caused 100% death of Opisthorchis 72 hours later. In golden hamster experiments, the efficiency of the aspen bark extract was 73.48-83.0%. Butanolic and ethylacetatic extracts were found to have the greatest antiopisthorchiatic activity. The results of chemical and chromatographic studies indicated that active fractions contained salicine and its derivatives. The aspen bark extract produces no substantial toxic effect on laboratory animals and belongs to the class "Low-toxic substances".

Protection against chemical-induced lung injury by inhibition of pulmonary cytochrome P-450.

Protection afforded by trialkyl phosphorothionates against the lung injury caused by trialkyl phosphorothiolates probably results from the inhibition by the P = S moiety of the thionates, of one or more pulmonary cytochrome P-450 isozymes. The aromatic hydrocarbons p-xylene and pseudocumene also protect against this injury and inhibit some P-450 isozymes, but by a different mechanism. OOS-Trimethylphosphorothionate and p-xylene were compared as protective agents against the effect of OOS-trimethylphosphorothiolate and two other lung toxins ipomeanol and 1-nitronaphthalene that are known to be activated by cytochrome P-450. The effects of these protective compounds, in vivo, on pulmonary cytochrome P-450 activity were also determined. Both compounds inhibited pentoxyresorufin O-deethylase activity, but not ethoxyresorufin O-deethylase. The phosphorothionate was most effective against lung injury caused by the phosphorothiolates and 1-nitronaphthalene, whereas p-xylene was much more effective against ipomeanol. beta-Naphthoflavone, which induces pulmonary ethoxyresorufin O-deethylase activity, did not protect against phosphorothiolate or 1-nitronaphthalene injury, and it was only marginally effective in decreasing the toxicity of ipomeanol.