(1S*,4aR*,5S*,6S*,8aR*)-3-Benzyl-1-methyl-5,6-diphenyl-3,4,4a,5,6,8a-hexa­hydro-1H-2,3-benzoxazin-4-one

In the title compound, C28H27NO2, the oxazinone ring adopts a twist-boat conformation and the cyclo­hexene ring has a twisted envelope conformation. The crystal structure is stabilized by weak non-classical inter­molecular C—H⋯O hydrogen bonds

Effect of healthy Qigong “WuQinXi” exercise on peripheral blood T-cell subgroups in middle-aged subjects

“WuQinXi” is becoming a popular exercise among elders. This study measured the peripheral blood Tcell subgroups in elderly “WuQinXi” practitioners. Fifty healthy Chinese people (male 15, female 35), aged between 50 and 69, attended a 135 min Tai Chi practice session four times a week for three months. The results showed significant (P < 0.05, P < 0.01) differences in peripheral blood T-cell subgroups between before and after exercise. The improvement noted in the “WuQinXi” practitioners may reflectincreased ratio of CD4+ to CD8+. Moreover, the effect was better in female practitioners than male ones. This data suggest that “WuQinXi” exercise may improve immunity function of elderly practitioners

3-(1,3-Dithio­lan-2-yl­idene)-1-(4-meth­oxy­phen­yl)pyridine-2,4(1H,3H)-dione

In the title compound, C15H13NO3S2, the dithiol­ane ring adopts a twisted conformation. The mol­ecule exhibits a V-shaped conformation, with a dihedral angle of 79.05 (7)° between the benzene ring and the pyridine ring. In the crystal, C—H⋯O inter­actions are observed

Aspirin-triggered lipoxin A4 attenuates LPS-induced pro-inflammatory responses by inhibiting activation of NF-κB and MAPKs in BV-2 microglial cells

<p>Abstract</p> <p>Background</p> <p>Microglial activation plays an important role in neurodegenerative diseases through production of nitric oxide (NO) and several pro-inflammatory cytokines. Lipoxins (LXs) and aspirin-triggered LXs (ATLs) are considered to act as 'braking signals' in inflammation. In the present study, we investigated the effect of aspirin-triggered LXA₄(ATL) on infiammatory responses induced by lipopolysaccharide (LPS) in murine microglial BV-2 cells.</p> <p>Methods</p> <p>BV-2 cells were treated with ATL prior to LPS exposure, and the effects of such treatment production of nitric oxide (NO), inducible nitric oxide synthase (iNOS), interleukin-1β (IL-1β) and tumour necrosis factor-α (TNF-α) were analysed by Griess reaction, ELISA, western blotting and quantitative RT-PCR. Moreover, we investigated the effects of ATL on LPS-induced nuclear factor-κB (NF-κB) activation, phosphorylation of mitogen-activated protein kinases (MAPKs) and activator protein-1 (AP-1) activation.</p> <p>Results</p> <p>ATL inhibited LPS-induced production of NO, IL-1β and TNF-α in a concentration-dependent manner. mRNA expressions for iNOS, IL-1β and TNF-α in response to LPS were also decreased by ATL. These effects were inhibited by Boc-2 (a LXA₄receptor antagonist). ATL significantly reduced nuclear translocation of NF-κB p65, degradation of the inhibitor IκB-α, and phosphorylation of extracellular signal-regulated kinase (ERK) and p38 MAPK in BV-2 cells activated with LPS. Furthermore, the DNA binding activity of NF-κB and AP-1 was blocked by ATL.</p> <p>Conclusions</p> <p>This study indicates that ATL inhibits NO and pro-inflammatory cytokine production at least in part via NF-κB, ERK, p38 MAPK and AP-1 signaling pathways in LPS-activated microglia. Therefore, ATL may have therapeutic potential for various neurodegenerative diseases.</p

Hepatocarcinoma Angiogenesis and DNA Damage Repair Response: An Update

Hepatocarcinoma is one of the most common lethal human malignant tumors, mainly because of active angiogenesis. This kind of high angiogenesis often accounts for early metastasis, rapid recurrence, and poor survival. Growing evidence has proved that hepatocarcinoma angiogenesis is closely associated with multiple risk factors, such as DNA damages resulting from hepatitis B and C virus infection, aflatoxin B1 exposure, ethanol intake, and obesity. Genetic alterations and genomic instability, probably resulting from low DNA damage repair response (DRR) and the following unrepaired DNA lesions, are also increasingly recognized as important risk factors of hepatocarcinoma angiogenesis. Dysregulation of DRRs and signaling to cell cycle checkpoints involving in DRR pathways may accelerate the accumulation of DNA damages and trigger the dysregulation of angiogenesis-related genes and the progression of hepatocarcinoma. In this review, we discussed DNA damages/DRRs and angiogenesis during hepatocarcinogenesis and their interactive regulations. Hopefully, the review will also remind the medical researchers and clinic doctors of further understanding and validating the values of DNA damages/DRRs in hepatocarcinoma angiogenesis

1-Methyl-3-trifluoro­methyl-1H-pyrazol-5-ol

In the title compound, C5H5F3N2O, the F atoms are disordered over two sets of sites in a 0.64 (3):0.36 (3) ratio. In the crystal structure, O—H⋯N hydrogen bonds link the mol­ecules into chains and a short C—H⋯F contact also occurs