This study examined in vitro effect of lipoxin A 4 (LXA 4) on interleukin-1β (IL-1β) production of monocytes and its possible mechanism in severe preeclampsia (PE).Peripheral venous blood was drawn from 15 patients ...This study examined in vitro effect of lipoxin A 4 (LXA 4) on interleukin-1β (IL-1β) production of monocytes and its possible mechanism in severe preeclampsia (PE).Peripheral venous blood was drawn from 15 patients with severe preeclampsia (PE group) and 20 normal pregnant women (control group) to prepare monocytes which were then treated with LXA 4 at different concentrations of 0,10,100 nmol/L respectively.IL-1β level in the supernatant of monocytes was detected by enzyme linked immunoassay.The [Ca 2+ ] i of monocytes was measured by laser scanning confocal microscopy.The results showed that the IL-1β level and the [Ca 2+ ] i of monocytes in the PE group were significantly higher than those in the control group.LXA 4 significantly decreased the generation of IL-1β in a dose-dependent manner in the PE group.After treatment with 100-nmol/L LXA 4,in the PE group,the [Ca 2+ ] i concentration of monocytes was significantly reduced.It was concluded that LXA 4 may inhibit the IL-1β production of monocytes from severe preeclampsia women by inhibiting extracellular calcium influx.展开更多
AIM:Excessive dissolve of corneal tissue induced by MMPs which were activated by cytokins and chemokines will lead to corneal ulcer. The molecular mechanism of Lipoxin A4 (LXA4) on corneal collagen degradation in thre...AIM:Excessive dissolve of corneal tissue induced by MMPs which were activated by cytokins and chemokines will lead to corneal ulcer. The molecular mechanism of Lipoxin A4 (LXA4) on corneal collagen degradation in three dimensions was investigated. ·METHODS:Rabbit corneal fibroblasts were harvested and suspended in serum -free MEM. Type I collagen, DMEM, collagen reconstitution buffer and corneal fibroblast suspension were mixed on ice. The resultant mixture solidified in an incubator, after which test reagents and plasminogen was overlaid and the cultures were returned to the incubator. The supernatants from collagen gel incubations were collected and the amount of hydroxyproline in the hydrolysate was measured. Immunoblot analysis of MMP-1,-3 and TMMP-1,-2 was performed. MMP-2, -9 was detected by the method of Gelatin zymography. Cytotoxicity assay was measured. RESULTS:LXA4 inhibited corneal collagen degradation in a dose and time manner. LXA4 inhibited the IL -1β induced increases in the pro-MMP-1, -2, -3, -9 and active MMP -1,-2,-3,-9 in a concentration dependent manner. LXA4 also inhibited the IL-1β induced increases in TIMP-1, -2. CONCLUSION:As a potent anti-inflammation reagent, LXA4 can inhibit corneal collagen degradation induced by IL-1β in corneal fibroblasts thus inhibiting corneal dissolving pathology process.展开更多
文摘This study examined in vitro effect of lipoxin A 4 (LXA 4) on interleukin-1β (IL-1β) production of monocytes and its possible mechanism in severe preeclampsia (PE).Peripheral venous blood was drawn from 15 patients with severe preeclampsia (PE group) and 20 normal pregnant women (control group) to prepare monocytes which were then treated with LXA 4 at different concentrations of 0,10,100 nmol/L respectively.IL-1β level in the supernatant of monocytes was detected by enzyme linked immunoassay.The [Ca 2+ ] i of monocytes was measured by laser scanning confocal microscopy.The results showed that the IL-1β level and the [Ca 2+ ] i of monocytes in the PE group were significantly higher than those in the control group.LXA 4 significantly decreased the generation of IL-1β in a dose-dependent manner in the PE group.After treatment with 100-nmol/L LXA 4,in the PE group,the [Ca 2+ ] i concentration of monocytes was significantly reduced.It was concluded that LXA 4 may inhibit the IL-1β production of monocytes from severe preeclampsia women by inhibiting extracellular calcium influx.
基金Jilin University Basic Scientific Research Operating Expenses Fund, China (Research Fund of the Bethune B Plan of Jilin University, 2012 No.2012230)Research Fund of Jilin Provincial Science and Technology Department, China (international cooperation item, No.20120726)
文摘AIM:Excessive dissolve of corneal tissue induced by MMPs which were activated by cytokins and chemokines will lead to corneal ulcer. The molecular mechanism of Lipoxin A4 (LXA4) on corneal collagen degradation in three dimensions was investigated. ·METHODS:Rabbit corneal fibroblasts were harvested and suspended in serum -free MEM. Type I collagen, DMEM, collagen reconstitution buffer and corneal fibroblast suspension were mixed on ice. The resultant mixture solidified in an incubator, after which test reagents and plasminogen was overlaid and the cultures were returned to the incubator. The supernatants from collagen gel incubations were collected and the amount of hydroxyproline in the hydrolysate was measured. Immunoblot analysis of MMP-1,-3 and TMMP-1,-2 was performed. MMP-2, -9 was detected by the method of Gelatin zymography. Cytotoxicity assay was measured. RESULTS:LXA4 inhibited corneal collagen degradation in a dose and time manner. LXA4 inhibited the IL -1β induced increases in the pro-MMP-1, -2, -3, -9 and active MMP -1,-2,-3,-9 in a concentration dependent manner. LXA4 also inhibited the IL-1β induced increases in TIMP-1, -2. CONCLUSION:As a potent anti-inflammation reagent, LXA4 can inhibit corneal collagen degradation induced by IL-1β in corneal fibroblasts thus inhibiting corneal dissolving pathology process.
