Role of interleukin-1 in induction of matrix metalloproteinases synthesized by rat temporomandibular joint chondrocytes and disc cells.

To identify cartilage-degrading enzymes and cell types that can be specifically induced by interleukin-1 (IL-1)alpha, we studied matrix metalloproteinase (MMP) activities of cultured rat temporomandibular joint (TMJ) chondrocytes and disc cells. The cells were isolated from TMJs pre-injected with normal physiological saline (CR) or recombinant human IL-1alpha (AR). MMP activities in the conditioned media were assayed by gelatin enzymography, and they were identified by Western blot analyses. MMP mRNAs in these cells were also detected by RT-PCR. IL-1alpha significantly induced an increase of active MMP9 as well as pro- and active MMP3, but had no effect on the MMP2 activity in both types of cells. MMP3 and MMP9 mRNAs were also inducible in these cells by IL-1alpha stimulation. Furthermore, disc cells were more susceptible to IL-1alpha than chondrocytes. AR cells spontaneously produced the same MMPs in vitro as the CR cells synthesized under IL-1alpha stimulation. The results indicate that MMP9 and MMP3 were predominantly produced by disc cells, and these may be considered to play a pivotal role in ECM degradation during pathological conditions of the TMJ, such as IL-1-induced TMJ arthritis.

Cis- and trans-linalool 3,7-oxides and methyl salicylate glycosides and (Z)-3-hexenyl beta-D-glucopyranoside as aroma precursors from tea leaves for oolong tea.

Two new alcoholic aroma precursors, cis- and trans-linalool, 3,7-oxides 6-O-beta-D-apiofuranosyl-beta-D-glucopyranosides (1 and 2), as well as two already known compounds, (Z)-3-hexenyl beta-D-glucopyranoside (3) and methyl salicylate 6-O-beta-D-xylopyranosyl-beta-D-glucopyranoside (beta-primeveroside: 4), and another new monoterpendiol glycoside, 8-hydroxygeranyl beta-primeveroside (5) have recently been isolated as aroma precursors in tea leaves (Camellia sinensis var. sinensis cv. Maoxie) ready for oolong tea processing.

The effects of R-75,317 on antiglomerular basement membrane glomerulonephritis in rats.

Platelet-activating factor (PAF) is a potent inflammatory mediator which is released by various inflammatory cells and produced by certain tissues, including the kidney. PAF has been shown to increase glomerular permeability to protein and to decrease glomerular filtration rate (GFR) by contracting mesangium. On the basis of these observations, it has been suspected that PAF may play a role as mediator of glomerular damage in glomerular nephritis. To examine this possibility, we studied the effects of a specific PAF antagonist, R-75,317, on the development of an experimental model of anti-glomerular basement membrane (anti-GBM) glomerulonephritis. Glomerulonephritis was initiated by injecting rabbit anti-rat GBM serum into rats. Proteinuria gradually developed after serum injection, plateaued at week 2, and remained at the high level of week 2 throughout the experimental period (6 wk). Chronic treatment with R-75,317 (10 mg/kg/day i.p.) tended to delay the onset of proteinuria and significantly accelerated the recovery phase. Creatinine clearance (Ccr) fell to 40% at week 3. R-75,317 treatment completely prevented this decline of Ccr. Histological changes in this model (glomerular hypertrophy, proliferation of mesangial matrix and interstitial fibrosis) were also ameliorated by the R-75,317 treatment. The results suggest that PAF may play a role in the development of glomerulonephritis and that PAF antagonists could be used in the treatment of human renal disease.