- [Show abstract] [Hide abstract] ABSTRACT: CD4(+)Foxp3(+) regulatory T cells (Tregs) are required for normal immune homeostasis. Recent studies suggested that Treg transfer facilitates recovery from acute kidney injury (AKI), but the molecular events that maintain Treg function after adoptive transfer remain unclear. This study aimed to investigate the regulation of mammalian target of rapamycin (mTOR) signaling in the Treg-mediated therapeutic effect on ischemic AKI. We noted significant Treg expansion in C57BL/6 mouse kidney, with enhanced immunosuppressive capacity after renal ischemia/reperfusion. mTOR inhibition significantly increased the frequency of Tregs in cultured CD4(+) T cells, with enhanced production of anti-inflammatory cytokines, which, conversely, was reduced by mTOR activation. Rapamycin, an inhibitor of mTOR, was transiently administered to C57BL/6 mice before ischemia/reperfusion surgery. No beneficial effect of rapamycin treatment was seen in the early recovery of AKI as a result of its inhibitory effect on tubular regeneration. However, rapamycin markedly enhanced the expansion of kidney Tregs, with increased mRNA expression of anti-inflammatory cytokines. Adoptive transfer of rapamycin-treated Tregs markedly suppressed conventional T cells, responder myeloid cells, and reactive myofibroblasts; however, it promoted host Tregs and alternative macrophages, leading to better renal function and less kidney fibrosis. Taken together, Treg transfer with mTOR inhibition markedly improves outcomes of ischemic AKI. These findings reveal an important role for mTOR signaling in maintaining Treg activity after adoptive transfer and highlight the therapeutic potential of targeting Tregs in acute and chronic kidney disease.
- [Show abstract] [Hide abstract] ABSTRACT: Background: High blood glucose is characteristic of diabetic nephropathy (DN). Both lectin-like ox-LDL receptor-1 (LOX-1) and renal tubular epithelial cells apoptosis reportedly are important for the pathogenesis and progression of DN. In this study, we explored the regulatory effects of high glucose on the expression of LOX-1 and its impact on oxLDL-induced apoptosis in human renal proximal tubular epithelial cells (HRPTEpCs). Methods: Primary HRPTEpCs were treated with high glucose with or without concurrent treatment with selective p38 mitogen-activated protein kinase (MAPK) inhibitor PD169316 or lentiviral knockdown of LOX-1. HRPTEpCs cultured in normal glucose concentration (5.5 mmol/l) was used as a control. Results and conclusion: High glucose concentration dependency increased the expression of LOX-1, which led to increased ox-LDL binding in HRPTEpCs. In addition, high glucose upregulated the LOX-1 gene promoter activity but not its mRNA stability in HRPTEpCs; the effect was abolished by PD169316. Furthermore, high glucose markedly enhanced oxLDL-induced apoptosis in HRPTEpCs, which was largely abolished by knockdown of LOX-1. This study demonstrates that high glucose induces the expression of LOX-1 at the gene promoter/transcription level mainly by a p38 MAPK-dependent mechanism, which enhances oxLDL-induced apoptosis in renal tubular epithelial cells. It adds new insights into the molecular mechanisms underlying DN.
- [Show abstract] [Hide abstract] ABSTRACT: To explore the role of protein phosphatase 2A (PP2A) in renal interstitial fibrosis by using rat model of unilateral ureteral obstructive (UUO) or cell model of human kidney proximal tubular epithelial (HK)-2 cells treated with transforming growth factor-β1 (TGF-β1). METHODS: 1) A total of 15 Sprague-Dawley rats were randomly divided into a sham group, a UUO group and an okadaic acid (OA) treated group (OA group) (n=5 in each group). The OA [30 μg/(kg·d)], diluted with 1.8% alcohol, was given to the rats in the OA group through gastric tube after at 72 h after the surgery, while the equal volume of 1.8% alcohol was given to the rats in the sham group and the UUO group. After sacrificing rats, the blood and kidney were collected to detect the renal function and the expression of PP2Ac, fibronectin (FN), collagen-I (Col-I), E-cadherin (E-cad) and α-smooth muscle actin (α-SMA) by immunohistochemistry, Western blot and RT-PCR, respectively; 2) The likely concentration of OA was determined by Trypan blue dye exclusive assay and methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay. The HK-2 cells were incubated with serum-free Dulbecco's modified eagle medium (DMEM) for 24 h; then they were divided into a control group, a TGF-β1 group (treated with 5 ng/mL TGF-β1 for 24 h) and a TGF-β1+OA group (treated with 5 ng/mL TGF-β1 and 40 nmol/L OA for 24 h). The HK-2 cells were collected and the expression of PP2Ac, FN, Col-I, E-cad and α-SMA were detected by Western blot. RESULTS: 1) Compared with the sham group, the BUN and Scr in the UUO group increased (both P<0.05); compared with the UUO group, the BUN and Scr in the OA group decreased (both P<0.05); the expression of PP2Ac, FN, Col-I and α-SMA was up-regulated while the expression of E-cad was down-regulated in the UUO group compared with those in the sham group (all P<0.05). The expression of PP2Ac, FN, Col-I and α-SMA was down-regulated while the expressions of E-cad was up-regulated in the OA group compared with those in the UUO group (all P<0.05); 2) The likely concentration of OA was 40 nmol/L. Western blot showed that the expression of PP2Ac, FN, Col-I and α-SMA was up-regulated while the expressions of E-cad was down-regulated in the TGF-β1 group compared with those in the control group (all P<0.05); the expression of PP2Ac, FN, Col-I and α-SMA were down-regulated while the expression of E-cad was up-regulated in the TGF-β1+OA group compared with those in the TGF-β1 group (all P<0.05). CONCLUSIONS: PP2A might be able to promote the renal interstitial fibrosis. .
- [Show abstract] [Hide abstract] ABSTRACT: Contrast-induced nephropathy (CIN) is considered the third leading cause of iatrogenic acute kidney injury in high-risk patients undergoing radiographic procedures. The main mechanism leading to CIN is medullary hypoxia due to decreased renal blood flow, secondary to renal artery vasoconstriction and direct tubular toxicity by contrast medium. Furthermore, experimental data suggests that an activated renin-angiotensin-aldosterone system (RAAS) plays a role in the pathophysiology of CIN. However, the role of RAAS blockers, including angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) in CIN is controversial. They have been reported to be effective in the prevention of CIN in previous studies, but some studies have concluded that they were associated with an increased risk of CIN, especially in patients with pre-existing renal impairment. In summary, there is no solid data to link ACE inhibitors and ARB to CIN, and larger randomised controlled trials are necessary to further investigate their role in the development of CIN. In this review, we discuss the pathophysiology of CIN, the role of RAAS on the development of CIN, and the effect of RAAS blockers on CIN. © 2014 S. Karger AG, Basel.
- [Show abstract] [Hide abstract] ABSTRACT: Objective: To evaluate the mortality and risk factors for acute kidney injury (AKI) in hospitalized patients by the risk, injury, failure, loss, end stage kidney disease (RIFLE) and acute kidney injury network (AKIN). Methods: We constructed a retrospective study of all AKI patients in the Second Xiangya Hospital of Central South University between February 2006 and January 2011. The diagnosis and classification of AKI were reconfirmed and categorized by RIFLE and AKIN criteria. To compare the clinical characteristics, mortality and associated risk factors in AKI patients by the RIFLE and AKIN stage, univariate analysis and multivariate logistic regression analysis were performed. Results: The patients were diagnosed as AKI by AKIN (n=1027) or by RIFLE criteria (n=1020). There was no significant difference in the hospital mortality, hospital length stay (days), or the proportion of complete recovery in each stage of AKI patients by RIFLE and AKIN (P>0.05). In the univariate analysis, age, pre-renal causes, proportion of hospital acquired AKI, mechanical ventilation, hypotension, the number of failed organs, acute tubular necrosis-index severity score (ATN-ISS), and the peak of serum potassium ion concentration were significantly higher in the non-survivors than in the survivors (P<0.05). Logistic regression analysis revealed that age older than 65, hospital acquired AKI, hypotension, number of failed organs, ATN-ISS scores, and the peak of serum potassium ion concentration were independent risk factors for hospital mortality. Conclusion: Both RIFLE and AKIN criteria have similar scientific value in assessing hospital mortality. AKI stage is associated with the recent prognosis of AKI patients.
- [Show abstract] [Hide abstract] ABSTRACT: Good self-management behaviors can control symptoms of the patients with osteoarthritis, improve the patients' joint function and quality of life. Patients' self-management behaviors have been impacted by disease knowledge, self-efficacy, emotional state, and social support. All the above factors should been taken into full consideration when intervening. Self-management program is an intervention mode which can improve patient self-management behaviors and promote patient health.
- [Show abstract] [Hide abstract] ABSTRACT: Epithelial-mesenchymal transition (EMT) is thought to contribute to the progression of renal tubulointerstitial fibrosis. Norcantharidin (NCTD) is a promising agent for inhibiting renal interstitial fibrosis. However, the molecular mechanisms of NCTD are unclear. In this study, a unilateral ureteral obstruction (UUO) rat model was established and treated with intraperitoneal NCTD (0.1 mg/kg/day). The UUO rats treated with NCTD showed a reduction in obstruction-induced upregulation of α-SMA and downregulation of E-cadherin in the rat kidney (P<0.05). Human renal proximal tubule cell lines (HK-2) stimulated with TGF-β1 were treated with different concentrations of NCTD. HK-2 cells stimulated by TGF-β1 in vitro led to downregulation of E-cadherin and increased de novo expression of α-SMA; co-treatment with NCTD attenuated all of these changes (P<0.05). NCTD reduced TGF-β1-induced expression and phosphorylation of Smad2/3 and downregulated the expression of Snail1 (P<0.05). These results suggest that NCTD antagonizes tubular EMT by inhibiting the Smad pathway. NCTD may play a critical role in preserving the normal epithelial phenotype and modulating tubular EMT.
- [Show abstract] [Hide abstract] ABSTRACT: Albumin induced epithelial-mesenchymal transition (EMT) of renal tubular cells through reactive oxygen species (ROS) pathway plays an important role in tubulointerstitial fibrosis. Cordycepin (3 -deoxyadenosine), a potential antioxidant, was demonstrated to have various pharmacological effects and could inhibit EMT of some cells. However, the role of cordycepin on albumin-induced EMT in renal tubular cells (HK2) is unclear. In this study, we investigated the effect of cordycepin on albumin-induced EMT of HK2 cells and its mechanisms. HK-2 cells were exposed to bovine serum albumin with or without pretreatment with cordycepin. Results showed that albumin significantly induced EMT formation of HK-2 which associated with NADPH oxidase activation and intracellular ROS overproduction through increased Rac1 activity and expression of NOX4, p22phox and p47phox, while these effects were abolished in that pretreated with cordycepin. In conclusion, cordycepin could ameliorate albumin-induced EMT of HK2 cells by decreasing NADPH oxidase activity and inhibiting ROS production.
- [Show abstract] [Hide abstract] ABSTRACT: To investigate the role of oxidative stress in the epithelial-to-mesenchymal transdifferentiation (EMT) of peritoneal mesothelial cells in rat model of peritoneal fibrosis and the effect of probucol on peritoneal fibrosis. The rat model of peritoneal fibrosis was induced by 4.25% high glucose peritoneal dialysis fluid (PDF). The rats were randomly divided into 4 groups:the control group, the saline group, the peritoneal fibrosis group, and the probucol group. A 4 hour peritoneal equilibration test (PET) was performed 4 weeks later. The peritoneal function and net ultrafiltration (UF) volume were determined. The level of malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) in peritoneal tissue were examined. The histology of peritoneal membrane was evaluated by light microscopy. E-cadherin and α-smooth muscle actin (α-SMA) protein expression was evaluated by immunohistochemical method and Western blot. The mesothelial cells were detached from peritoneal membrane in peritoneal firbosis rats. Comparing with the control rats, the thickness of visceral peritoneum, the level of MDA, and the-SMA protein expression were increased while the net ultrafiltration volume, the level of GSH-Px and E-cadherin protein expression were decreased in peritoneal firbosis rats. All these changes were reversed in the rats treated with probucol. Oxidative stress plays an important role in transdifferentiation of peritoneal mesothelial cell in the peritoneal fibrosis rats. Probucol can improve structure and function of peritoneum, and partially reverse the EMT by reducing the oxidative stress.
- [Show abstract] [Hide abstract] ABSTRACT: To construct the cell model of epithelium to mesenchymal transition of proximal tubule cells induced by high glucose and to determine the expression of Smad anchor for receptor activation (SARA). Protein expression of vimentin, Zona occludens-1(ZO-1), and SARA was determined by Western blot, and their mRNA expressions were detected by Real-time PCR. After stimulation by 30 mmol/L D-glucose, the protein and mRNA expression levels of vimentin in HK-2 cells increased in a time-dependent manner while the expression of ZO-1 was reduced significantly, especially at 48 h. Meanwhile, SARA was also decreased in a time-dependent manner. High glucose can induce renal epithelium to mesenchymal transition, and SARA may be involved in this process as a protector.
- [Show abstract] [Hide abstract] ABSTRACT: High-glucose-based peritoneal dialysis solution (PDS) is considered to be one of the primary causes for the increase of ionic permeability in peritoneum as detected by transmesothelial electrical resistance (TER) measurements and claudin-1 expression. However, the mechanism is not clear. The aim of this study is to test the hypothesis that high-glucose PDS induces hyperpermeability in human peritoneal mesothelial cell (HPMC) monolayer by mitochondrial respiratory chain complex III pathway. HPMCs were cultured in a 1 : 1 mix of Dulbecco's modified Eagle's medium (DMEM) and PDS containing 1.5% and 4.25% glucose for 24 h. A 1 : 1 mixture of 160 mg/L glutathione and 4.25% glucose PDS was also added as an antioxidant group. TER measurement and immunostaining and western blot analysis of claudin-1 expression were examined for detection of permeability damage in HPMCs. MitoSOX™ Red staining and respiratory chain complexes' activities were determined for detection of mitochondrial reactive oxygen species (ROS) production and mitochondrial complexes' activities. TER decreased in a time- and concentration-dependent manner after culture with high-glucose PDS for 24 h. Claudin-1 was also downregulated. Complex III activity was inhibited accompanied by increasing mitochondrial ROS generation. These changes were partially prevented by glutathione. These findings demonstrate that mitochondrial respiratory complex III pathway has crucial importance in maintaining permeability of HPMCs, which might reveal a valuable target for novel therapies to fight hyperpermeability of peritoneum during the prolonged PD treatment.
- [Show abstract] [Hide abstract] ABSTRACT: Aims: The present study investigated the relationship between mast cells (MCs) and the protein expression of stem cell factor (SCF) and transforming growth factor-β1 (TGF-β1) in the regions of renal interstitial fibrosis with protein-overload nephropathy, in order to provide a good animal model to study the mechanism of renal fibrosis induced by proteinuria. Methods: 60 male Sprague-Dawley rats were divided into a bovine serum albumin (BSA) group and a control group. The intensity of MCs infiltration was examined by toluidine blue and chymase and tryptase staining. The protein expression of SCF and TGF-β1 was respectively examined by immunohistochemical and immunofluorescence staining. Results: Severe proteinuria was induced in rats of the BSA group. Expression of SCF and TGF-β1 was detected in the tubular and the interstitial cells. The number of MCs positively correlated with the severity of interstitial lesions and the expression of SCF and TGF-β1. Conclusion: Our results demonstrated that in protein-overload nephropathy, MCs infiltrated into the kidney, and the expression of SCF and TGF-β1 gradually increased. They might play important roles in the development of renal interstitial fibrosis, but the underlying mechanism needs to be further studied.
- [Show abstract] [Hide abstract] ABSTRACT: To determine the effect of 2 transforming growth factor beta1 (TGF-beta1) short hairpin RNA (shRNA) expression plasmids (pcDU6-A1-A2 and pcDU6-B1-B2) on proliferation, TGF-beta1, connective tissue growth factor (CTGF), and fibronectin (FN) expression induced by human serum albumin (HSA) in HK2 cells. A vector plasmid containing the TGF-beta1 shRNA was generated. An HK2 cell line was used in the study. The 2 TGF-beta1 shRNA expression plasmids were transfected into cultured HK2 cells by lipofectamine 2000. Cellular proliferation was assessed by tetrazolium salt colorimetry. The semi-quantitative reverse transcriptive PCR was performed to detect the expression of TGF-beta1, CTGF, and FN mRNA. Levels of TGF-beta1 and FN protein were measured with a sandwich enzyme-linked immunosorbent assay. After treating with 5 g/L HSA for 24 hours in HK2 cells, cellular proliferating capacity increased significantly (P<0.05). The expression levels of TGF-beta1, CTGF, and FN mRNA were upregulated in HK2 cells stimulated by 5 g/L HSA, and levels of TGF-beta1 and FN protein in the culture supernatant increased (P<0.05). The introduction of pcDU6-A1-A2 and pcDU6-B1-B2 resulted in significant reduction of cellular proliferation activity, and the expression levels of TGF-beta1, CTGF, and FN mRNA were downregulated (P<0.05). Levels of TGF-beta1 and FN protein in the culture supernatant decreased (P<0.05) after 12 or 24 hours of TGF-beta1 shRNA transfection into HK2 cells There was no significant difference in the expression levels of TGF-beta1, CTGF, and FN mRNA between the 2 pcDU6 vector plasmid mediated TGF-beta1 shRNA groups (P>0.05). pcDU6 vector plasmid mediated TGF-beta1 shRNAs could obviously inhibit the expression levels of TGF-beta1, CTGF, FN and cellular proliferation stimulated by HSA in HK2 cells, which may be related to the mediation of TGF-beta1.
- [Show abstract] [Hide abstract] ABSTRACT: To determine the incidence and risk factors associated with acute kidney injury (AKI) in patients after cardiac surgery with extracorporeal circulation. A retrospective case control study was done in patients who underwent cardiac surgery from 2003 to 2007 in Second Xiangya Hospital, with 340 patients in an AKI group and the other 4 760 patients without AKI as a control group. All variables were analyzed by univariate analysis, Mann-Whitney U test and logistic regression. AKI occurred in the 340 patients (6.7% incidence). Univariate analysis revealed that age, preoperative serum creatinine, preoperative ejection fraction (EF), preoperative beta2-microglobulin, preoperative blood albumin, preoperative blood uric acid, intraoperative cardiopulmonary bypass time, intraoperative aortic cross-clamp time, and dosage of mannitol were significantly related to AKI following cardiac surgery with extracorporeal circulation. Logistic multivariate regression analysis showed that preoperative serum creatinine (P<0.001), preoperative ejection fraction (EF) (P<0.001), preoperative beta2-microglobulin (P=0.002), preoperative blood uric acid (P=0.015), intraoperative cardiopulmonary bypass time (P<0.001), and intraoperative aortic cross-clamp time (P<0.001) were independent risk factors for AKI. The incidence of AKI after cardiac surgery with extracorporeal circulation is closely related with a variety of perioperative risk factors. Our data suggest that patients planning to accept cardiac surgery with extracorporeal circulation should be more comprehensively assessed and monitored, thereby preventing the occurrence of AKI.
- [Show abstract] [Hide abstract] ABSTRACT: To investigate the effect of different concentrations of glucose peritoneal dialysates (PDS) on monolayer transmesothelial electrical resistance (TER) and migration ability of cultured human peritoneal mesothelial cells (HPMCs) to clarify the cause of peritoneal hyperpermeability state and ultrafiltration failure during prolonged peritoneal dialysis. HPMCs were cultured in a 1:1 mixture of DMEM and PDS containing 1.5%, 2.5%, and 4.25% glucose. Methyl thiazolyl tetrazolium (MTT) assay and TER were measured to determine the effect of glucose PDS on the proliferation and permeability of human peritoneal mesothelial monolayers, respectively. Wound-healing assay was used to confirm whether glucose could do harm to the migration of cells. Proliferation of HPMCs was significantly suppressed by different glucose concentrations at 24 hours. TER decreased in a time- and concentration-dependent manner after culture with different concentrations of glucose PDS. Cells lost migration in the presence of high glucose after 24 hours, and most cells lost their normal morphology and became detached from plates after 48 hours of wounding. High glucose in PDS can cause peritoneal damage by suppressing cell proliferation, inducing increase in paracellular permeability of HPMCs and inhibiting cell migration after damage, which may be responsible for peritoneal hyperpermeability and the development of ultrafiltration failure.
- [Show abstract] [Hide abstract] ABSTRACT: To summarized the experiences from our basic experimental and clinical research on peritoneal dialysis. In the past 16 years, peritoneal fibrosis rat models and rabbit models of peritonitis were first established successfully in our laboratory in China. Peritoneal mesothelial cells were also separated and identificated. Besides, we assessed the biocompatibility of peritoneal dialysis fluid and analyzed the molecular mechanism of peritoneal mesothelial cell injury. We demonstrated the key role of transforming growth factor-beta1 (TGF-beta1), connective tissue growth factor (CTGF) and peroxisome proliferative activated receptor-gamma (PPAR-gamma) in the pathogenesis of peritoneal fibrosis, as well as their regulation of molecular mechanism. Furthermore, we transfected the plasmids encoding TGF-beta1-shRNA or pCTGF-shRNA into peritoneal cells and tissues by nanocarrier technologies. In clinical research, the positioning of peritoneal dialysis catheters, peritoneal dialysis treatment modalities and the prevention and treatment of its complications were studied. The characteristics and mechanism of solute transport in peritoneal dialysis was also explored.
- [Show abstract] [Hide abstract] ABSTRACT: Radiocontrast-induced nephropathy is a clinically important complication of intravascularly applied radiocontrast media. A predominant toxic effect of contrast media on renal tubules has been shown in previous clinical trials and animal experiments. Bax and Bcl-2 are members of the Bcl-2 family. Caspases are a family of cell death proteases, caspase-3 is one of the key executioners of apoptosis. In this study, we evaluated the cytotoxicity of high-osmolar contrast media (HOCM; diatrizoate) and low-osmolar contrast media (LOCM; iohexol) on human renal tubular epithelial cells (HKCs), and determined the regulatory roles of Bax/Bcl-2 and caspase-3 on apoptosis induced by contrast media (CM) in HKCs. An HKC line was used. Experiments were divided into 7 groups: the HOCM group with iodine 111 mg/mL, HOCM group with iodine 74 mg/mL, LOCM group with iodine 111 mg/mL, LOCM group with iodine 74 mg/mL, mannitol high-osmolar control group, mannitol low-osmolar control group and a culture media control group . The cytotoxicity of HOCM and LOCM were evaluated by cell proliferation and viability assay (MTT assay) and lactate dehydrogenase (LDH) release. Apoptosis were assessed by Hochest 33258 fluorescence-stained cytospins, TUNEL staining, DNA agarose gel electrophoresis, electron microscope and flow cytometric DNA analysis. The protein ex-pression of Bax/Bcl-2 was determined by Western blot analysis, and caspase-3 activity was also determined by the fluo-rometric method. Compared with the control group, LDH levels increased significantly (p<0.05) and cell viability decreased in cells treated with HOCM or LOCM (p<0.05) in an osmotic pressure-, iodinated ion- and time-dependent manner; in the HOCM groups, diatrizoate induced cultured HKC apoptosis. In the LOCM groups, iohexol did not induce apoptosis. Compared with equal osmotic pressure mannitol, apoptosis increased in HKCs incubated with diatrizoate (p<0.05). Bax/Bcl-2 production and caspase-3 activity were up-regulated in cultured HKCs treated with HOCM iodine 74 or 111 mg/mL meglumine diatrizoate. Both HOCM and LOCM had toxic effects on HKCs, HOCM was more cytotoxic than LOCM; HOCM induced cultured HKC apoptosis while LOCM did not induce cultured HKC apoptosis in the indicated concentrations. The regulation of apoptosis induced by HOCM in HKCs may be regulated by Bax/Bcl-2 and caspase-3.
- [Show abstract] [Hide abstract] ABSTRACT: The objective was to investigate the relationship between homocysteine (HCY), peroxisome proliferator-activated receptors (PPAR)-gamma and the expression of interleukin 6 (IL-6) and microsomal prostaglandin E synthase (mPGES) by peripheral blood mononuclear cell (PBMC) culture in vitro, as well as to look at the intervention with HCY and PPAR-gamma activators (troglitazone and rosiglitazone). PBMC were isolated from venous blood of normal volunteers and incubated with HCY and PPAR-gamma activator of varying concentrations for 24 hr. The supernatant of the culture medium was collected in order to determine the IL-6 and mPGES levels by ELISA assay. The results show that the expression of IL-6 and mPGES in the HCY experimental group was significantly higher than that in the control group (p<0.01 and p<0.05, respectively). Additionally, the IL-6 and mPGES levels rose with the increase of HCY in a dose-dependent manner (p<0.01 and p<0.05, respectively). PPAR-gamma activator could significantly inhibit the increase of IL-6 and mPGES induced by 100 micromol/L HCY (p<0.05 and p<0.01, respectively). In conclusion, HCY can increase the expression of IL-6 and mPGES, while PPAR-gamma activator can inhibit the increase of IL-6 and mPGES induced by HCY.
Central South University
Ch’ang-sha-shih, Hunan, China
- Institute of Neurology