[show abstract][hide abstract] ABSTRACT: Receptor activator of nuclear factor-kB ligand (RANKL), a well-known membrane-bound molecule expressed on osteoblasts and bone marrow stromal cells, is believed to induce osteoclast differentiation and activation by binding to the receptor activator of nuclear factor-kB (RANK), which is expressed on the surface of osteoclast lineage cells. This induction is inhibited by osteoprotegerin (OPG) that is secreted by osteoblast lineage and acts as a decoy receptor of RANKL. Currently the essential role of the OPG/RANKL/RANK system in the process of osteoclast maturation, as well as activation, has been well established, and the majority of bone resorption regulators control osteoclast formation and activation through their effects on this system and especially on the relative expression levels of RANKL and OPG .
[show abstract][hide abstract] ABSTRACT: To develop an intermittent hypoxia/reoxygenation (IH/ROX) rabbit carotid artery model and then investigate the inflammation status of rabbit carotid artery endothelium after IH exposure and its relationship with leptin.
After anesthetization, rabbit's right common carotid artery was cleared of surrounding tissue with anatomic microscope, cannulated to its distal part and the proximal part was ligated. Preparations were challenged by changing the PO(2) of the gas mixture equilibrating the perfusate. Alternate perfusing (2 mL/min) of equilibrated perfusate bubbled with normoxia or hypoxia gas mixtures formed IH/ROX cycles in the right carotid common artery, simulating the pattern of hypoxic episodes seen in obstructive sleep apnea (OSA), or continuous perfusing of hypoxia perfusate to form continuous hypoxia (CH) modes. Sixty adult male New Zealand White rabbits (2.5-3.0 kg) were separated into six groups, ten per group. Groups were: A, intermittent normoxia (IN) group, perfused with perfusion equilibrated with 21% O(2) [PO(2) about 141 +/- 2.87 mmHg] for 15 s and 21% O(2) for 1 min 45 s, 60 cycles; B, severe IH group, 5% O(2) [PO(2) about 35.2 +/- 1.27 mmHg] 15 s and 21% O(2) 1 min 45 s, 60 cycles; C, mild IH group, 10% O(2) [PO(2) about 54.3 +/- 3.31 mmHg] 15 s and 21% O(2) 1 min 45 s, 60 cycles; D, severe IH+Lep group, protocol was the same with severe IH group; E, CH group, IN for 1 h 45 min and then 5% O(2) for 15 min; and F, Lep group, the same with IN group. Right common carotid artery parts distal to the cannula were harvested after exposure, and endothelial cell layers were gotten from longitudinal outspread vessels. Nuclear factor kappaB (NFkappaB) DNA binding activities of partial cell layers were measured with electrophoretic mobility shift assay in the IN group, severe IH group, mild IH group, and CH group nuclear extracts. The other part of the cell layers in the IN group, severe IH group, severe IH+Lep group, and Lep group were cultured for 2 h, and during the culture procedure, recombinated human leptin solutions were added to culture dishes of severe IH+Lep group and Lep group (resulted concentration, 10 ng/mL). Enzyme-linked immunosorbent assay was used to analyze medium interleukin-6 (IL-6) concentrations, reverse transcription polymerase chain reaction was used to analyze endothelial cell Ras homology A (RhoA) mRNA expression levels. Statistical analysis was done with SPSS 11.5 software package.
NFkappaB DNA binding activities were significantly different between groups (F = 112.428, P < 0.001). This activity in the severe IH group (4.27 +/- 0.64) was higher than that in the mild IH group (2.33 +/- 0.45, P < 0.001), IN group (1.00 +/- 0.26, P < 0.001), and CH group (1.15 +/- 0.36, P < 0.001). RhoA mRNA expression levels were different in groups (F = 26.634, P < 0.001).This level in the severe IH+Lep group (2.54 +/- 0.53) was higher than that in the severe IH group (1.57 +/- 0.44, P = 0.002), IN group (1.00 +/- 0.31, P < 0.001), and Lep group (1.31 +/- 0.30, P < 0.001). IL-6 concentrations were different in groups (F = 79.922, P < 0.001). IL-6 concentration in the severe IH+Lep group (1591.50 +/- 179.57 pg/mL) was higher than that in the severe IH group (1217.20 +/- 320.62 pg/mL, P = 0.036), IN group (325.40 +/- 85.26 pg/mL, P < 0.001), and Lep group (517.40 +/- 183.09 pg/mL, P < 0.001).
IH/ROX activated the inflammation pathway significantly in the endothelium, which was more intensive than CH and intensity-dependent. When exposed to both IH/ROX and leptin, inflammation occurs more dramatically. It means that synergic activating roles were performed by IH/ROX and leptin. This study may have a clinical implication that IH can cause endothelial damage through activated inflammation in OSA patients, and if the OSA patients have obesity at the same time, the endothelial damage or the inflammation would be more significant because of elevated leptin level as a synergic factor.
Sleep And Breathing 03/2009; 13(3):277-83. · 2.26 Impact Factor
[show abstract][hide abstract] ABSTRACT: Osteoclast inhibitory lectin (OCIL) is a novel regulator of bone remodeling, however, little is known concerning how OCIL is regulated to date. In this study, approximately 4.4 kb of the 5'-flanking sequence of rat OCIL gene was cloned into the promoter-less reporter vector pGL3-basic and transiently transfected into three different cell lines. The differences in the levels of luciferase activity paralleled well with the levels of OCIL mRNA expression in these cells, suggesting that the regulation of rat OCIL gene expression occurs mainly at the transcriptional level. Additional luciferase assays using a series of constructs containing unidirectionally deleted fragments showed that the construct-1819/pGL3 (-1819 to +118) exhibited the highest luciferase activity, suggesting the presence of functional promoter in this region. The region from -4370 to -2805 might contain negative regulatory elements, while the region from -1819 to -1336 might have important positive regulatory elements that enhance OCIL transcription. Sequence analysis of the promoter revealed the absence of both TATA and CAAT boxes. However, in the proximal promoter region (-81 to +118), several potential transcription factor binding sites that may be responsible for the basal transcriptional activity of rat OCIL promoter were observed. The promoter contains several potential Sp1 binding sites, and cotransfection of a shRNA expression plasmid that knockdowns Sp1 significantly reduced OCIL promoter activity and endogenous gene expression and moreover, overexpressing Sp7, a Sp1 family member that also binds to Sp1 binding sequence, increased OCIL promoter activity and gene expression, suggesting a role of Sp1 family proteins in regulation of OCIL transcription.
Journal of Cellular Biochemistry 02/2009; 106(4):599-607. · 3.06 Impact Factor
[show abstract][hide abstract] ABSTRACT: Osteoclast inhibitory lectin (OCIL) is a recently identified inhibitor of osteoclast formation. A variety of osteotropic factors regulate OCIL expression in osteoblastic cells, however, little information is available to date concerning how this gene is controlled. Using real-time RT-PCR, we examined the regulation of OCIL expression by PTHrp and the signaling pathways used. We demonstrated in rat osteoblast-like UMR-106 cells, rat calvarial primary osteoblastic cells, and murine MC3T3-E1 cells, PTHrp(1-34) increased OCIL expression. In UMR-106 cells, the increase began and reached maximum later than RANKL induction and OPG suppression. cAMP/PKA signaling activators PTH(1-31), forskolin and dibutyryl cAMP (db-cAMP), and calcium ionophore A23187 all increased OCIL levels. In contrast, PKC activator phorbol-12-myristate-13-acetate reduced OCIL expression in short term but induced OCIL mRNA in long term. PKA inhibitor KT5720, mitogen-activated protein kinase (MAPK) cascade inhibitor PD98059, calmodulin antagonist W-7, and Ca(2+)/calmodulin-dependent protein kinase II (CaMK II) inhibitor KN-62 all significantly blunted PTHrp-stimulated OCIL expression. Moreover, PD98059 blocked the stimulation of OCIL by FSK or db-cAMP but not that by A23187. In primarily cultured osteoblasts, the PTHrp induction of OCIL was blocked by KT5720, W-7, and PD98059 as well. The data established that PTHrp(1-34) regulates OCIL expression in vitro through cAMP/PKA, Ca(2+)/CaMK II, and MAPK signaling pathways.
[show abstract][hide abstract] ABSTRACT: To explore the inflammatory reactions, endothelin level and carotid sinus nerve (CSN) afferent activity of carotid body (CB) after intermittent hypoxia/reoxygenation (IH/ROX) exposure of various frequencies in rabbits.
Forty-nine male adult New Zealand white rabbits (2.5-3.0 kg) were separated into 7 groups (n = 7 each). After anesthetization, the right carotid artery and CSN were cleared of surrounding tissues without touching the right CB and the left carotid region. The CSN was unenveloped to partially expose the myelin sheath, and electrodes were placed to the "single" chemoreceptor bundle of the CSN, with CSN afferent activity carefully monitored and recorded. Then the right common carotid artery was exposed, cannulated to distal part and its proximal part was ligated. Preparations were challenged by changing the PO2 of the gas mixture equilibrating the perfusate. Alternatively perfusion (2 ml/min) of equilibrated perfusate bubbled with normoxia or hypoxia gas mixtures formed IH/ROX cycles in right carotid common artery, simulating the pattern of hypoxic episodes seen in obstructive sleep apnea, or with continuously perfusing hypoxia perfusate to form continuous hypoxia (CH) modes. Groups were defined with different frequencies, and groups were: intermittent normoxia group (IN group) (21% O2, 15 s; 21% O2, 1 min 45 s), 10/hr group (5% O2, 15 s; 21% O2, 5 min 45 s), 30/hr group (5% O2, 15 s; 21% O2, 1 min 45 s), 50/hr group (5% O2, 15 s; 21% O2, 57 s), 60/hr group (5% O2, 15 s; 21% O2, 45 s) and 90/hr group (5% O2, 15 s; 21% O2, 25 s). All the above groups were exposed to 60 treatment cycles; continuous hypoxia group (CH group), IN for 1 h 45 min and then 5% O2 for 15 min. After exposure and 30 min of static placing, CSN afferent frequencies (Charge F) were recorded from chemoreceptor bundles, and the right CB was cleared of surrounding tissues and harvested. Interleukin-6 (IL-6), endothelin-1 (ET-1), hypoxia-inducible factor-1 (HIF-1), and vascular endothelial growth factor (VEGF) concentrations of the CB lysate were measured with enzyme linked immuno sorbent assay (ELISA) kits and standardized. Data were analyzed with SPSS 12.0 software package; and after one way analysis of variance (ANOVA) for whole difference, Tamhane's T2 was used for post hoc analysis.
IL-6, ET-1 and Charge F increased but then decreased with increasing IH frequencies (F = 25,601.39, 2390.48, 6945.84, all P values < 0.01). IL-6, ET-1 and Charge F levels in 50/hr group were the highest among groups. Charge F levels correlated significantly with IL-6 or ET-1 (with IL-6: r = 0.736, P < 0.01; with ET-1: r = 0.757, P < 0.01, respectively). IL-6, ET-1 and Charge F levels between IN group and CH group were not statistically different (all P values > 0.05). HIF-1 levels elevated gradually (F = 5241.10, P < 0.01) with increasing exposure frequencies, and the CH group had the highest value (all P values < 0.01). VEGF level in CH group was the highest in all groups (all P values < 0.01).
After IH/ROX exposure, afferent activity of CB CSN increases, which significantly correlates with inflammation and vasomotor mechanism of CB. CB inflammation comes not from IH phases but from ROX phases. Increased CB CSN activity results in elevated SNA tension, which plays a key role in the pathogenesis of systemic hypertension. This procedure influenced by IH/ROX frequencies. CH for 15 min causes no definitely damages. However, HIF-1 and VEGF can be considered as members of adaptive pathway during IH/ROX exposure.
Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases 09/2008; 31(9):670-4.
[show abstract][hide abstract] ABSTRACT: cDNAs of certain target genes are difficult to obtain by traditional reverse transcription. Herein we describe a novel method to synthesize cDNA based upon the use of the class IIS restriction enzymes. Briefly, the exons of a certain gene are separately PCR-amplified, each using the primers containing a recognition sequence of a certain class IIS restriction enzyme. All the fragments are restricted using the enzyme(s), resulting in the cohesive end of each exon that is complementary to the one in its adjacent exon. Then the fragments can be assembled together in their naturally occurring order. We successfully applied this method to acquire the coding sequence of Hoxa7 gene. This approach is simple, highly efficient, less error prone and cost-effective, and can also be used to fuse different PCR-fragments from distinct genes to create a chimeric gene or to perform site-directed mutagenesis.
[show abstract][hide abstract] ABSTRACT: To investigate the regulation of receptor activator of nuclear factor kappaB ligand (RANKL) and osteoprotegerin (OPG) mRNA expression by prostaglandin E2 (PGE2) in osteoblastic-like cells and involved signaling pathways.
Rat UMR106 osteoblast-like cells were cultured and treated with various dose of PGE2 or regulators of different signaling pathways such as protein kinase A, protein kinase C, ERK-MAPK and calcium/calmodulin pathways for different period of time,the cells were then harvested at indicated time points, total RNA were isolated and RANKL/OPG mRNA expression were studied by real-time PCR.
PGE2, Forskolin and db-cAMP increased RANKL mRNA by 2.8 times (P = 0.002), 2.2 times (P = 0.006) and 2.1 times (P = 0.005) respectively, and inhibited OPG mRNA expression by 12% (P < 0.01), 85% (P = 0.005) and 70% (P = 0.013) respectively, while RANKL and OPG mRNA expression were down-regulated by A23187 by 58% (P = 0.002) and 53% (P = 0.017) respectively. As for inhibitory experiments, the stimulatory effects of PGE2 on RANKL mRNA expression could be inhibited only by KT-5720 by 53% (P < 0.01), while the other inhibitors did not have any effect at all. The inhibitory effects of PGE2 on OPG mRNA expression were partially blocked by KT-5720 by 47% (P = 0.01), verapamil by 38% (P = 0.029) and W7 by 43% (P < 0.01) respectively, while KN-62, chelerythrine and PD98059 had no effects.
PGE2 can up-regulate the expression of RANKL but down-regulate the expression of OPG. The up-regulation of RANKL mRNA expression by PGE2 was mediated through the activation of PKA signaling pathway while PGE2 induced down-regulation of OPG mRNA expression was predominantly mediated via PKA as well as the Ca2+ /Calmodulin signaling pathways.
[show abstract][hide abstract] ABSTRACT: Traditional strategies for establishing shRNA expression constructs are inefficient, error-prone, or costly. We describe a simple approach that overcomes these drawbacks. Briefly, the sense and antisense strands of the short hairpin RNA coding sequence are segmented into two parts, respectively, at asymmetric sites. The four resulting short oligonucleotides are synthesized. Each oligonucleotide is annealed with its opposite, resulting in a double-stranded fragment with sticky termini at both ends. The two fragments so generated can be easily spliced by simple ligation to reconstitute the full-length short hairpin RNA coding sequence which can then be cloned into an appropriately restricted vector.
[show abstract][hide abstract] ABSTRACT: We have developed a novel protocol for site-directed mutagenesis of double-stranded DNA. The procedure, termed SORS (named because it undergoes the sequential procedure of segmentation-overhang creating PCR-reannealing-splicing) mutagenesis, is exemplified by a substitution, a deletion, and an insertion of nucleotide(s) in target genes. The template DNA is PCR-amplified into two separate segments divided at the prospective mutation site, and each segment is amplified in two parallel PCRs using primers introducing the mutation. The primers are designed to be able to create protruding bases upon pooling, denaturing, and reannealing the two parallel reactions. The protruding bases at the prospective junction of the two segments are mutually complementary; therefore, the two segments can be re-spliced together to generate the mutated gene. Compared to previously published protocols, this procedure is rapid, restriction-independent and ensures higher success rate and lower potential to produce second-site mutations.
[show abstract][hide abstract] ABSTRACT: To observe the effect of overdose iodine on the expression of CCK gene in brains of rats and identify the possible mechanisms.
One-month weaning Wistar rats were randomly divided into five groups which were fed with normal feedstuff and water supplemented with different concentrations of potassium iodide, named A group (iodine ration was about 6.15 microg per day), B group (iodine ration was about 30.75 microg per day), C group (iodine ration was about 61.5 microg per day), D group (iodine ration was about 307.5 microg per day) and E group (iodine ration was about 615 microg per day). Rats were sacrificed after being fed for three or six months. Then serum thyroid hormones were measured by radioimmunoassay and the mRNA level of CCK gene was studied by using RT-PCR technique.
At the end of three months, the values of thyroid hormones in E group [TT4 (45.2 +/- 13.7) nmol/L, TI'3 (0.65 +/- 0.20) nmol/L, FT3 (0.93 +/- 0.45) pmol/L, FT4 (7.07 +/- 2.43) pmol/L, rT3 (0.15 +/- 0.04) nmol/L] were all lower than those in A group [TT4 (76.0 +/- 18.8) nmol/L, TT3 (1.34 +/- 0.41) nmol/L, FT3 (2.45 +/- 0.62) pmol/L, FT4 (15.12 +/- 3.40) pmol/L, rT3 (0.24 +/- 0.04) nmol/L]. There were significant differences between E group and A group on the levels of serum TH (F values are 14.68, 16.03, 21.16, 20.25, 13.52 respectively, P < 0.01); FT3 levels in C and D groups were significantly decreased as compared to A and B groups (F = 21.16, P < 0.05). rT3 level in D group was significantly decreased compared with A,B and C groups (F = 13.52, P < 0.05). At the end of six months, the levels of serum TH in E group (TT4 (51.84 +/- 15.83) nmol/L, TT3 (0.77 +/- 0.22) nmol/L, FT4 (6.88 +/- 2.23) pmol/L, FT3 (0.74 +/- 0.28) pmol/L, rT3 (0.14 +/- 0.03) nmol/L) were lower than those in any other groups (F values were 6.05, 12.22, 11.25, 13.42, 5.89 respectively, P < 0.05). At the end of both three and six months, the mRNA levels of CCK gene in E group were lower than any other groups (F values were 4.04, 3.95 respectively, P < 0.01). The results of correlation analysis showed that serum FT4 had linear correlation with levels of CCK mRNA (r values were 0.990, 0.948 respectively; P < 0.05); However serum FT3 had no linear correlation with the levels of CCK mRNA (r values are 0.970, 0.932 respectively).
Exposure to overdose of iodine (iodine ration was 100-fold higher than that of A group) could decrease the mRNA level of CCK gene. Compared with FT3, FT4 might have more important role on the regulation of CCK mRNA induced by excess of iodine.
Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine] 04/2008; 42(3):173-6.
[show abstract][hide abstract] ABSTRACT: We have developed a novel protocol for directional cloning of PCR products into any vector. The target sequence is amplified in two parallel asymmetric PCRs using specially but simply designed primers. Two single-stranded products are produced and they are annealed to form a double-stranded DNA fragment bearing overhangs at both ends that correspond to the restriction overhangs of certain restriction enzymes. The fragment can then be cloned into a certain vector previously treated with the corresponding enzymes without restriction of the inserted fragment. Compared with previously published protocols, the procedure described in this paper is highly efficient and it is independent of the restriction sites of the insert and is therefore applicable to molecular biology and biotechnology studies.
[show abstract][hide abstract] ABSTRACT: The recent identification of receptor activator of nuclear factor-kappaB ligand (RANKL)/RANK/osteoprotegerin (OPG) cytokine system has led to a new molecular perspective on osteoclast biology and bone homeostasis. Specifically, the interaction between RANKL and RANK is responsible for osteoclast differentiation. In the present study, we evaluated whether soluble RANK (sRANK) could act as an antagonist of RANKL and down-regulate osteoclastogenesis and bone resorption in vitro. The prokaryotic expression vector coding for sRANK was constructed. Then the construct was introduced into E. coli Origami B (DE3) competent cells and recombinant sRANK was successfully produced and purified through affinity chromatography. sRANK reduced osteoclast-like cell (OLC) formation and resorption pit formation induced by parathyroid hormone (PTH) in a dose-dependent manner. In addition, sRANK significantly inhibited PTH-induced mRNA expression of carbonic anhydrase II and tartrate-resistant acid phosphatase in murine bone marrow cells as confirmed by using semi-quantitative RT-PCR. The down-regulation was highly correlated with the effect of sRANK on OLC formation from marrow cells. These data demonstrate the anti-resorptive effects of sRANK in vitro and highlight the potential of sRANK as a novel therapeutic approach to bone disorders characterized by enhanced bone resorption.
Sheng li xue bao: [Acta physiologica Sinica] 05/2007; 59(2):169-74.
[show abstract][hide abstract] ABSTRACT: To study the therapeutic effects of Rhizoma Drynariae and estrogen on osteoporosis in ovariectomized (OVX) rats.
Fifty-five female rats were randomly divided into 5 groups, the normal control (normal),the sham operated (sham), the model, the estrogen, and the Rhizoma drynariae (RD) groups; ovariectomized rats were used as postmenopausal osteoporosis model. The changes of morphology and dynamic parameters in different groups were determined by bone histomorphometry.
Compared with the model group, the trabecular volume (TBV/TTV) , trabecular thickness (MTPT) and density (MTPD) in the other four groups were significantly increased, while the trabecular template spacing (MTPS) and the ratio of trabecular surface to trabecular volume (TBS/TBV) significantly decreased (P <0. 05); and the osteoid surface (TOS), single label surface [Sfract (s) ] ,double label surface [Sfract (d) ] and bone formation rate (Svf) also decreased,while osteoid maturation period (OMP) increased in the latter four groups. No significant difference of cortical width (MCW) was found between these 5 groups. Compared with the normal and sham groups, TOS, Sfract ( s) , Sfract ( d) , Svf in the estrogen and RD groups increased significantly, while OMP decreased; no significant difference was found in other parameters.
Rhizoma Drynariae has the similar effect with estrogen in maintaining normal trabecular structure and connection by inhibiting the increased bone turnover of postmenopausal osteoporosis.
Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine / Zhongguo Zhong xi yi jie he xue hui, Zhongguo Zhong yi yan jiu yuan zhu ban 06/2006; 26 Suppl:116-9.
[show abstract][hide abstract] ABSTRACT: Osteoprotegerin ligand (OPGL) is a key regulator of formation and activation of osteoclasts. In the present study, the cDNA encoding the extracellular domain of murine OPGL (sOPGL) was synthesized by RT-PCR and cloned into fusion expression vector pET-42a(+) in a certain strategy on purpose that the fusion tag could be completely removed by factor Xa from the expressed fusion protein without any vector-encoded sequence left. Induced with IPTG, the recombinant E. Coli cells produced a 47 kD protein in high level that could be recognized, through Western blotting analysis, by the antibody against OPGL. The expressed products were purified through Glutathione-sepharose 4B affinity chromatography. Along with the fusion molecule, a protein about 30 kD was also specifically bound to the resin. The 30 kD molecule could be recognized by polyclonal antibody against GST-IGF-1, but not by antibody against OPGL. It suggested that the 30 kD molecule was derived from the degradation of the fusion protein. After the cleavage with factor Xa and further purification, the fusion tag was removed and the recombinant sOPGL was obtained. Finally, we confirmed that the recombinant sOPGL could promote osteoclast formation from mouse bone marrow cells in a dose dependent manner.
[show abstract][hide abstract] ABSTRACT: To clarify the effects of nylestriol on microarchitecture and interleukin-6 (IL-6) mRNA expression in tibial bone in ovariectomized rats.
30 female rats were randomly allocated into 3 groups: sham, OVX and nylestriol-treated group. Nylestriol-treated group were ovariectomized, then fed with nylestriol for 3 months and the bone mineral density (BMD) was measured in lumbar vertebra by dual energy x-ray absorptiometry. After sacrifice of the animal, bone histomorphometric parameters were measured to study the changes in bone microarchitecture, and RT-PCR was performed to detect the expression of IL-6 mRNA in bone tissue.
BMD was significantly reduced, while IL-6 mRNA level elevated in the OVX group compared with the sham group. Static histomorphometric data showed that the trabecular bone volume, mean trabecular plate thickness and density were reduced while the mean trabecular plate space elevated remarkably in the OVX group in comparison with that in the sham group. As for dynamic parameters, trabecular osteoid surface, tetracyclin labeled surface and bone turnover rate were increased while osteoid maturation rate decreased significantly in the OVX group compared with the sham group. BMD, IL-6 mRNA expression and bone histomorphometric parameters were improved in nylestriol-treated rats.
Nylestriol plays an important role in maintaining bone volume and improving bone microarchitecture by markedly inhibiting bone turnover and bone resorption, which might be to some degree attributed to reduced IL-6 expression.
Zhonghua bing li xue za zhi Chinese journal of pathology 07/2004; 33(3):255-9.