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1.
AIM: To investigate the effect of microRNA-132 (miR-132) transfection on the lipopolysaccharide (LPS)-induced inflammation in rat alveolar macrophages. METHODS: The rat alveolar macrophage NR8383 cultured without pyrogen in vitrowere divided into blank control group, negative control group and transfected group. The cells in the 3 groups were transfected with phosphate buffer solution (PBS), Lipofectamine 2000 and synthesized miR-132 mimic respectively. The cell proliferation was detected by Cell Counting Kit-8 (CCK-8) assay. Real-time PCR was used to detect the expression of miR-132 in the cells. After NR8383 cells were stimulated with LPS for 6 h, the NF-κB DNA-binding activity was measured by electrophoretic mobility shift assay (EMSA). The expression of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in NR8383 cells was assayed by Western blotting.RESULTS: After transfection, the expression of miR-132 was significantly higher than that in blank control group and negative control group. The growth of NR8383 cells in transfected group was significantly inhibited compared with blank control group and negative control group (P<0.05). After the cells were stimulated with LPS, the productions of NF-κB, TNF-α and IL-6 in transfected NR8383 cells were decreased compared with blank control group and negative control group (P<0.05).CONCLUSION: Transfection of alveolar macrophages with miR-132 significantly suppresses the cell growth, and inhibits inflammatory responses induced by LPS.  相似文献   

2.
AIM:To investigate the effect of microRNA-181a (miR-181a) on cigarette smoke extract (CSE)-induced autophagy disorder and releases of pro-inflammatory factors in NR8383 rat alveolar macrophages. METHODS:The NR8383 cells were treatment with 5%,10% and 20% CSE. The release levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-8 were measured by ELISA. The level of miR-181a was detected by RT-qPCR. The numbers of autophagosomes were observed by Cyto-ID staining. The expression levels of LC3-Ⅱ, beclin-1 and p62 were determined by Western blot. NR8383 cells were pretreated with autophagy inhibitor 3-methyladenine (3-MA) or autophagy agonist rapamycin (Rapa) before treatment with 20% CSE, and the release levels of TNF-α, IL-6 and IL-8 were measured by ELISA. Furthermore, NR8383 cells were transfected with miR-181a mimic or miR-181a inhibitor before treatment with 20% CSE, and the release levels of TNF-α, IL-6 and IL-8, and the expression of LC3-Ⅱ, beclin-1 and p62 were detected by ELISA and Western blot, respectively. RESULTS:CSE increased release levels of pro-inflammatory factors and autophagy disorder in a concentration-dependent manner in the NR8383 cells (P<0.05). 3-MA increased CSE-induced releases of pro-inflammatory factors. However, Rapa partially reversed CSE-induced releases of pro-inflammatory factors. Additionally, miR-181a mimic inhibited CSE-induced releases of pro-inflammatory factors and promoted autophagy. However, miR-181a inhibitor increased CSE-induced releases of pro-inflammatory factors and autophagy disorder. CONCLUSION:miR-181a regulates CSE-induced releases of pro-inflammatory factor in the NR8383 cells, which may be related to the regulatory role of miR-181a in autophagy disorder.  相似文献   

3.
AIM: To explore the effects of sodium ferulate (SF) on function of macrophages in colonic tissue of the colitis rats in vivo. METHODS: The immunological colitis model of rats was produced. SF was used intracolonically for 21 days. The contents of malondialdehyde (MDA), nitric oxide (NO), prostaglandin E2 (PGE2) and the activity of superoxide dismutase (SOD), interleukin-1 (IL-1), TNF-α, myelopexoxidase (MPO), and the expression level of NF-κB p65 in colonic tissue of the rats were detected. RESULTS: SF (200,400,800 mg/kg) decreased the elevated contents of MDA, NO, PGE2, the activity of IL-1, TNF-α, MPO, and the expression level of NF-κB p65, while increased the reduced activity of SOD in colonic tissue of the colitis rats in a dose-depended manner. CONCLUSION: SF restrained the activity of activated colonic macrophages and relieved the colonic inflammation reaction in vivo in colitis rats, which may be related to the suppression of NF-κB activation.  相似文献   

4.
AIM: To explore the effects of aflatoxin G1(AFG1 )on proliferation and TNF-α secretion of human peripheral blood mononuclear cells(HPBM) in vitro. METHODS: The effects of AFG1 on proliferation of HPBM were analysed with flow cytometric (FCM) DNA analysis and MTT bioassay, while that on TNF-α secretion was detected with ELISA.RESULTS: FCM analysis revealed that 6 h after treatment, proliferation index(PI) of 1000 μg/L AFG1 treated HPBM was significantly higher than that of control. 24 h after AFG1 treatment, stimulating effects on proliferation was found in HPBM treated with AFG1 at 200 μg/L and 1 000μg/L.Regression analysis showed that PI was postively correlated with the concentrations of AFG1 in the concentration range from 0 to 1 000μg/L( r=0. 5122 and 0.5119 respectively,P＜0.05).MTT bioassay showed that the A value of the cells treated with AFG1 at 2 000 μg/L was higher than that of the control. Double antibody sandwich enzyme linked immunosorbent assay (ELISA) results showed that AFG1 at a dose of 100 μg/L could significantly inhibit lipopolysaccharide-induced TNF-α secretion.CONCLUSION: AFG1 could stimulate the proliferation of HPBM and could decrease TNF-α secretion at certain concentration.  相似文献   

5.
AIM: To investigate the possible mechanism of resveratrol (Res) on tumor necrosis factor-α (TNF-α)-induced monocyte chemoattractant protein-1 (MCP-1) expression in primary rat pulmonary artery endothelial cells (RPAECs).METHODS: RPAECs were randomly divided into 4 groups:control group, solvent (1% DMSO) group, TNF-α group and Res group. Each group was divided into 1 h, 4 h and 8 h subgroups (n=6 per time point). The TNF-α+C1142 (a rodent chimeric mAb that neutralizes rat MCP-1) group was set up at the 8 h time point. At each time point, the protein and mRNA expression of MCP-1 was measured by Western blot and real-time PCR.RESULTS: Pretreatment of the RPAECs with C1142 significantly down-regulated the expression of MCP-1 (P<0.05). The protein and mRNA expression of MCP-1 was markedly increased in TNF-α group (P<0.05). Notably, incubation with Res down-re-gulated the protein and mRNA expression of MCP-1, which was significantly lower than that in TNF-α group (P<0.05).CONCLUSION: MCP-1 was involved in the process of TNF-α-induced injury of RPAECs. Res down-regulates the expression of MCP-1 in RPAECs, thus attenuating cell injury.  相似文献   

6.
AIM: To explore the effects of lipoxin A4 on the expression of cyclooxygenase 2 (COX-2) in human bronchial epithelial cells (HBECs). METHODS: HBECs were incubated with various concentrations (0.1, 1 and 10 mg/L) of lipopolysaccharide(LPS) for 9 h, or 1 mg/L LPS for different time (3 h, 6 h and 9 h). The levels of COX-2 mRNA in HBECs and prostaglandin E2 (PGE2) in the culture supernatant were measured. In addition, the HBECs were exposed to lipoxin A4 at concentration of 0, 100 and 400 μmol/L after stimulated with LPS at concentration of 1 mg/L for 9 h, and the supernatant of the culture cells was collected for determining the content of PGE2 by ELISA. The cells were also harvested, and the mRNA and protein levels of COX-2 were analyzed by RT-PCR and Western blotting, respectively. RESULTS: LPS increased the mRNA expression of COX-2 and production of PGE2 in a dose and time dependent manners in HBECs. Induction of COX-2 mRNA and protein by LPS were inhibited by lipoxin A4 in a dose-dependent manner. Lipoxin A4 also significantly decreased LPS-induced production of PGE2. CONCLUSION: Lipoxin A4 down-regulates LPS-induced expression of COX-2 and consequently inhibits the production of PGE2 in HBECs.  相似文献   

7.
AIM：To investigate the effects of Xijiao Dihuang and Yinqiao San decoction (XDY) on the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in mouse lung tissues and rat pulmonary microvascular endothelial cells (RPMVECs) infected with influenza virus, and to explore its mechanism for treatment of viral pneumonia. METHODS：Fifty-four male BALB/c mice were randomly divided into normal group, model group and XDY group (n=18 in each group). The viral pneumonia model was established by intranasally dripping influenza A (H1N1) virus into the mice. The mice in XDY group were treated with XDY 1 h after dripping the virus. The expression of ICAM-1 and VCAM-1 in lung tissues was examined by immunohistochemical staining 2, 4 and 6 d after infection. On the other hand, RPMVECs were obtained from male Wistar rats and primarily cultured. The cells were randomly divided into control group, virus group, virus+XDY group, tumor necrosis factor α (TNF-α) group and TNF-α+XDY group. The mRNA and protein expression of ICAM-1 and VCAM-1 was evaluated by real-time PCR and flow cytometry 24 h after infection. RESULTS：Virus exposure increased ICAM-1 and VCAM-1 expression in mouse lung tissues (P<0.01), and XDY treatment attenuated this effect (P<0.01). Virus and TNF-α both led to the increases in mRNA and protein expression of ICAM-1 and VCAM-1 in RPMVECs (P<0.01), which were also reduced by treatment with XDY (P<0.01). CONCLUSION：Treatment with XDY decreases virus-induced ICAM-1 and VCAM-1 expression, suggesting an important role of XDY in treatment of viral pneumonia.  相似文献   

8.
AIM: To investigate the effects of extract of Ginkgo biloba (EGB) on the expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) induced by tumor necrosis factor a(TNF-α) in bovine aortic endothelial cells(BAECs). METHODS: The BAECs were incubated with TNF-α, followed by EGB treatment. The effect of EGB on LOX-1 expression was investigated by RT-PCR and Western blotting. The content of endothelial nitric oxide synthase (eNOS) was determined by Western blotting. Potential involvement of signaling pathways of the effects was explored by using related inhibitors of the signal molecules. The concentration of NO-2/NO-3 was also tested. RESULTS: Increased LOX-1 expression was induced by TNF-α. EGB markedly prevented the increase of LOX-1 expression induced by TNF-α (P<0.05), and this effect was inhibited by inhibitor of NOS (P<0.05). EGB significantly prevented the decrease of eNOS expression induced by TNF-α (P<0.05). EGB also significantly prevented the decrease of NO-2/NO-3 production induced by TNF-α (P<0.05). CONCLUSION: EGB markedly prevents the increase of LOX-1 expression induced by TNF-α and the effect is mediated by eNOS.  相似文献   

9.
AIM: To investigate the role of CD36 in casein-induced mouse renal injury.METHODS: Eight-week-old male C57BL/6J mice and CD36 knockout (CD36KO) mice were randomly divided into C57BL/6J saline injection group, C57BL/6J casein injection group and CD36KO casein injection group (n=8 in each group). After 14 weeks of treatment with high-fat diet, the mouse serum, 24 h urine and kidney tissue samples were collected for analysis. The serum content of tumor necrosis factor-α (TNF-α) was measured by ELISA. The renal function markers in the serum and urine were determined by an automatic biochemical analyzer. The pathological changes of the kidney were observed by HE staining and Masson staining. The expression of CD36 and cytokines/chemokines (TNF-α, IL-6 and MCP-1) at mRNA and protein levels in the renal tissues were determined by real-time PCR and Western blot. The content of tissue hydrogen peroxide (H2O2) was measured by a commercial kit. The protein levels of Nrf2 and TGF-β1 in the renal tissues were measured by immunohistochemical staining.RESULTS: Compared with saline injection group, casein injection increased the level of TNF-α in the serum and in the kidney tissues of C57BL/6J mice (P<0.05), suggesting that casein injection successfully induced chronic inflammation in C57BL/6J mice. Casein injection also promoted the protein expression of CD36 and TGF-β1 in the renal tissues of the C57BL/6J mice, accompanied with glomerular sclerosis, proteinuria, increased serum creatinine content, increased H2O2 content, and decreased Nrf2 protein level and the ability of antioxidant in the kidneys (P<0.05). Furthermore, CD36 deficiency protected the mice from casein-induced renal injury, as evidenced by improved kidney pathological changes and decreased proteinuria. The content of H2O2 in the kidneys of casein-treated CD36 knockout mice was also lower than that in casein-treated C57BL/6J mice.CONCLUSION: Inflammatory responses promote the oxidative stress and renal injury in a CD36-dependent manner.  相似文献   

10.
AIM: To investigate the effects of drynaria total flavonoids on serum levels of leptin (LEP), interleukin 6(IL-6), prostaglandin E2(PGE2) and the expression of bone β2-adrenergic receptor (ADRB2) in a rat model of ovariectomized osteoporosis(OP). METHODS: The osteoporosis model was established by ovariectomy. Twelve weeks after modeling,bone mineral density (BMD) was determined by dual-energy X-ray absorptiometry to verify successful modeling.Enzyme-linked immunosorbent assay was applied to detect the concentrations of LEP, IL-6 and PGE2 in serum. The expression of ADRB2 was determined by immunohistochemical technique. RESULTS: Compared with sham group,BMD of the rats in model group significantly decreased in multiple regions 12 weeks after modeling(P<0.01). The serum levels of LEP, IL-6 and PGE2 in model group were significantly higher than those in sham group(P<0.05). The levels of LEP, IL-6 and PGE2 in drynaria total flavonoids group were significantly lower than those in model group(P<0.01). No significant difference of PGE2 between these 2 groups was observed. The ADRB2 expression in sham group and treatment group was significantly different from that in model group, and no significant difference between sham group and treatment group was found. CONCLUSION: The serum levels of LEP, IL-6 and PGE2 and the expression of bone ADRB2 increased in OP rats.Drynaria total flavonoids reduce the production of LEP, IL-6 and the expression of ADRB2, and suppress the bone absorption, which may be one of the mechanisms in treating OP.  相似文献   

11.
AIM: To observe the effect of central prostaglandin E2 (PGE2) on sympathetic activation in chronic heart failure (CHF) and to explore the underlying mechanism. METHODS: Male SD rats were subjected to coronary artery ligation to induce heart failure (HF), and the intracerebroventricular infusion was performed by osmotic pump continuously. The rats in sham group and HF group were given artificial cerebrospinal fluid (0.25 μL/h). The rats in HF plus treatment group was given celecoxib (CLB; 20 mg/h). After 4 weeks, the levels of PGE2 in cerebrospinal fluid (CSF), the sympathetic nerve excitability and cardiac function were measured, and the changes of corticotropin-hormone releasing hormone (CRH)-containing neurons activation and neurotransmitter contents in the hypothalamic paraventricular nucleus (PVN) were also determined. RESULTS: Compared with the sham-operated rats, the HF rats had raised level of PGE2 in CSF, up-regulated renal sympathetic nerve activity and plasma norepinephrine, increased left ventricular end diastolic pressure, lung-to-body weight and right ventricular-to-body weight ratios, and decreased maximal increase and decreased rate of left ventricular pressure (P<0.05). In addition, the number of CRH positive neurons in PVN and the level of plasma adrenocorticotropic hormone were higher in HF rats than those in sham-operated rats (P<0.05). After administration of CLB into the lateral ventricle of HF rats, the contents of PGE2 in CSF were significantly reduced, the number of activation CRH neurons in PVN was decreased, the excitability of sympathetic nerves was down-regulated and cardiac function was improved (P<0.05). Compared with the sham-operated rats, the content of glutamic acid in PVN of HF rats was increased, the content of γ-aminobutyric acid and the number of glutamate decarboxylase 67-positive neurons were decreased (P<0.05). After the CLB was given, the above indexes were reversed (P<0.05). CONCLUSION: These findings indicate that in CHF, the increased central PGE2 may activate CRH-containing PVN neurons and contribute to the augmented sympathetic drive possibly by modulating the neurotransmitters within the PVN.  相似文献   

12.
AIM: To observe the immunoregulatory effects of prostaglandin E2 receptor (EP) subtypes EP2/EP4 on the B-cells of collagen-induced arthritic(CIA)mice. METHODS: DBA/1 mice were immunized with chicken type II collagen emulsified in Freunds complete adjuvant to induce arthritis. B-cells were isolated from the splenocyte suspension by positive selection using anti-CD19 monoclonal antibody immunomagnetic beads. The expression of MHC II, CD 80 and CD86 was examined by flow cytometry. The mRNA levels of EPs, interferon γ (IFN-γ), tumor necrosis factor α (TNF-α), IL-6, IL-4, IL-10 and transforming growth factor-β (TGF-β) were detected by real-time RT-PCR. RESULTS: The rank of the mRNA levels of EPs was EP2>EP1>EP3>EP4 in B-cells and EP2/EP4 mRNA expression was obviously increased in CIA mice. EP2 antagonists inhibited the expression of MHC II, CD80 and CD86. EP4 antagonist had little effect on CD80. EP2/EP4 antagonists inhibited the mRNA expression of IFN-γ, TNF-α, and IL-6 (P<0.05 or P<0.01) and increased the expression of IL-10 (P<0.01 or P<0.05). Furthermore, the antagonists of EP2 and EP4 also increased the mRNA expression of IL-4 and TGF-β (P<0.01), respectively. CONCLUSION: PGE2 modulate the pathogenesis of CIA via EP2/EP4 by regulating the expression of surface molecules and cytokines in B-cells. EP2/EP4 may be a new therapeutic target for treating rheumatoid arthritis.  相似文献   

13.
AIM: To investigate the effect of IL-10 on IL-1β-induced prostaglandin E2(PGE2) release and cyclooxygenase-2(COX-2) expression in human mesangial cells and to examine whether IL-10 has effect on the biological function of IL-1β.METHODS: The PGE2 concentration in supernatants of HMC was measured by radioimmunoassay. The COX-2 mRNA and protein were measured by RT-PCR and Western blot, respectively. RESULTS: PGE2 and COX-2 were significantly increased after treatment with IL-1β(P＜0.01 for both) in cultured human mesangial cells. IL-10 had no effects on basical production of COX-2 and PGE2(P＞0.05, respectively), while it inhibited IL-1β-elicited PGE2 production, as well as COX-2 mRNA and protein expression in a concentration-dependent fashion. CONCLUSIONS: These results indicated that IL-10 depressed the IL-1β-induced release of PGE2 and expression of COX-2. These data suggested that IL-10 could exert anti-inflammatory actions at several levels, not only by inhibiting the production of pro-inflammatory cytokines but also by suppressing their biological function.  相似文献   

14.
AIM: To observe the effects of losartan potassium on renal expression of transforming growth factor beta 1(TGF-β1), CD68 and monocyte chemoattractant protein-1 (MCP-1) in type 2 diabetic nephropathy rats for exploring the protective mechanism of losartan potassium on type 2 diabetic rat kidney. METHODS: Thirty Sprague-Dawley rats were randomized into 3 groups: normal control group, model group and treatment group. The morphology of kidney tissues, the renal function, and the change of 24 h urinary protein quantitative index were measured after 15 weeks of treatment, while TGF-β1, CD68 and MCP-1 expression in kidney cortex was observed by immunohistochemistry. RESULTS: Compared with the normal control rats, the body weight of the rats was lower in other groups, but the levels of blood glucose, triglyceride and cholesterol were higher.The expression of CD68, MCP-1 and TGF-β1, 24 h urinary protein quantitative index and serum creatinine were higher in model group than those in normal control rats. However, compared with model group, serum creatinine, 24 h urinary protein quantitative index and the expression of CD68, MCP-1 and TGF-β1 were decreased in treatment group. CONCLUSION: Losartan potassium protects the kidney of diabetic nephropathy rats through inhibiting the expression of TGF-β1 and MCP-1 in the kidney and restraining macrophage infiltration.  相似文献   

15.
AIM: To study the relationship between the activity of phospholipase A2 (PLA2) and pulmonary structural remodeling with the model of chronic isobaric hypoxic pulmonary hypertension. METHODS: 29 healthy Sprague-Dawley rats were randomly divided into normal control group, chronic hypoxic group and hypoxia plus Polidatin (PD) group. By diameter, the arteries were divided into two groups: arteries of group I (30 μm-100 μm) and group II (101 μm-200μm). The mean pulmonary arterial pressure (mPAP) was measured by inserting a microcatheter into the pulmonary artery. The PLA2 activity was measured with modified microtitrimetic method. The pulmonary tissue and arterioles morphology changes were examined under light microscope. RESULTS: It was found that after 21 days hypoxia, the mean pulmonary arterial pressure (mPAP), the PLA2 activity in blood and lung homogenate increased significantly. The media thickness of group I arteries increased (P<0.01) while that of group II arteries had no significant changes. The ratio of media area and adventitia of both groups was raised. Under light microscope, it was observed that pulmonary vascular endothelium proliferated, media became thickening and adventitia matrix increased. Pretreatment with PD could attenuate the changes mentioned above. CONCLUSION:PLA2 plays an important inducing role through promotion of the pulmonary vascular structural remodeling in the formation of chronic hypoxic pulmonary hypertension.  相似文献   

16.
AIM:To study the relationship between the activity of phospholipase A2 (PLA2) and chronic hypoxic pulmonary hypertension. METHODS:29 healthy SD rats were randomly divided into normal control group, chronic hypoxic group and hypoxia plus Polidatin (PD) group. The model of rat chronic hypoxic pulmonary hypertension was made by method of intermittent isobaric hypoxia for 21 days. The mean pulmonary arterial pressure (mPAP) was measured by inserting a microcatheter into the pulmonary artery. RESULTS:After exposing hypoxia for 21 days, the mPAP, R/L+S, the PLA2 activity, TXB2, MDA in plasma and lung homogenate increased significantly, while 6-k-PGF1α, SOD decreased significantly. Pretreatment with PD could relieve the changes mentioned above.CONCLUSION:PLA2 plays an important inducing role through its metabolic products and the interactional radicals in the formation of chronic hypoxic pulmonary hypertension.  相似文献   

17.
AIM: To investigate the effects of curcumin (Cur) on the expression of High mobility group box 1 protein (HMGB1), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) in amyloid-β (Aβ)-induced primary rat microglial cells. METHODS: Microglia were derived from the cerebral cortices of postnatal rat brains. The cells were identified by immunocytochemistry using mouse anti rat Iba-1 monoclonal antibody. A cell model using primary rat microglial cells incubated with Aβ25-35 as an inflammation model of Alzheimer's disease (AD) was set up. The morphological characters of primary rat microglial cells were observed. The concentration of Aβ25-35 and the treatment concentration of curcumin were selected by CCK-8 assay. Cultured primary rat microglial cells were divided into 5 groups:normal cell group, Aβ25-35 group, Cur group, Aβ25-35+Cur group and Aβ25-35+DMSO group. The expression of HMGB1, NF-κB, and receptor for advanced glycation end products (RAGE) was detected by Western blot. The levels of HMGB1, IL-1β, and TNF-α in the culture supernatant were measured by ELISA. RESULTS: The purity of primary microglias determined by Iba-1 immunofluorescence was more than 95%. The protein levels of HMGB1, RAGE and NF-κB were significantly increased after Aβ25-35 stimulation. After treatment with Cur, the protein levels of HMGB1, RAGE and NF-κB were significantly decreased (P<0.05). The levels of HMGB1, IL-1β and TNF-α in the supernatant were significantly increased after Aβ25-35 stimulation. Cur significantly decreased the level of HMGB1, IL-1β and TNF-α in the supernatant. CONCLUSION: Curcumin significantly inhibits neuroinflammation stimulated by Aβ25-35 in primary rat microglial cells.  相似文献   

18.
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19.
AIM: TO study the control mechanism of the developing of inflammation diseases, two inflammatory mediators, TNFa and arachidonic acid(AA) and its derivatives have been used as stimuli to induce human peripheral blood neutrophils to produce superoxide radicals. METHODS: The method of lucigeni - dependent light release has been used to exam the ability of releasing superoxide of neutrophils induced by the cooperation of TNFa and high class fatty acids as well as their derivatives. RESULTS: TNFa pretreatment markedly augmented the amount of superoxide produced in response to AA. Similarly, polyunsaturated fatty acids(PUFA) such as eicosapentaenoic acid, docosahexaenoic acid, linoleic acid, linlenic acid as well as monounsaturated fatty acid oleic acid were effected by TNFa. However, hydroxide (C20:4, n - 6 hydroxy) and hydroperoxide(C20:4, n - 6 hydroperoxy) of AA were not effected by TNFa. Leukotriene B4(LTB4) and PGE2 which are products of AA metabolism via the lipoxygenase and cyclooxygenase pathways respectively. The two major major of mediators are generated during an inflammatory response. The former acted on neutrophils in the generation of reactive oxygen species while the latter played an inhibition function. CONCLUSION: The complexity of the mediator network operating in various immune reactions and interaction between unsaturated lipids and cytokines may play an important role in disease processes and regulation of immune responses.  相似文献   

20.
AIM:To explore the role of tumor necrosis factor alpha(TNF-α) in the pathogenesis of liver fibrosis.METHODS:The proliferation and apoptosis of hepatic stellate cells (HSCs) in vitro were detected with flow cytometry, electron microscopy and TUNEL.RESULTS:The flow cytometry analysis showed that the cell proliferation index (PI) in the TNF-α(0.5 μg/L, 2.0 μg/L, 8.0 μg/L) groups was evidently lower than that in the control group (P＜0.05). In the cell cycle distribution, the portion of G0/G1 phase in the TNF-α groups was significantly higher than that in the control group(P＜0.05), but the portion of S phase in the TNF-α groups was evidently lower than that in the control group(P＜0.05). These indicated that TNF-α interfered with HSCs entrance into S phase from G0/G1 phase whereupon the proliferation of HSCs was inhibited. The apoptotic rate in the TNF-α groups was evidently higher than that in the control group(P＜0.05). The gene expression of bcl-2 and bax was also detected with flow cytometry. The expression of bcl-2 in the TNF-α groups was evidently lower than that in the control group(P＜0.05), but the expression of bax in the TNF-α groups was significantly higher than that in the control group(P＜0.05). TUNEL analysis showed the apoptotic rate of HSCs in the TNF-α(2.0 μg/L) group was 18.7%±2.5% compared with 5.3%±1.2% in the control group(P＜0.05).CONCLUSIONS:TNF-α interfered with HSCs entrance into S phase from G0/G1 phase whereupon the proliferation of HSCs was inhibited. TNF-α down-regulated bcl-2 gene expression and up-regulated bax gene expression whereupon the apoptosis of HSCs was induced.  相似文献   

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