Objective To investigate the effects of parathyroid hormone(PTH)on microinflammatory and nutritional status in maintenance hemodialysis(MHD)patients.Methods Ninety-eight MHD patients were selected,who hod undergone hemodialysis for at least three months before the study and were in a stable clinical status without signs of infection or disease activity.The serum level of intact PTH was measured by electrochemiluminescence immunoassay(ECLIA),while the serum levels of interleukin(IL)-1β,IL-6,IL-8 and tumor necrosis factor-α(TNF-α)were detected by enzyme-linked immunosorbent assay(ELISA).The levels of C-reactive protein(CRP),albumin(Alb),pre-albumin(PA),hemoglobin(Hb)and lipids were measured.Body measurement and modified quantitative subjective global assessment(MQSGA)was done simultaneously.Correlation analysis between serum PTH level and the parameters for inflammation and nutrition Was performed.Results The serum levels of intact PTH in MHD patients[(353.46±102.41)ng/L]were significantly higher than those in the control people[(57.45±5.76)ng/L,P<0.01],and the serum levels of IL-1β,IL-6,IL-8,TNF-α and CRP were significantly higher in MHD patients than those in the control people(P<0.01 or <0.05).Relative body weight(RBW),triceps skin fold thickness(TSF),mid-arm circumference(MAC)and mid-arm muscle circumference(MAMC)in MHD patients decreased significantly(P<0.05 or <0.01),while the score of MQSGA increased markedly(P<0.01).The levels of intact PTH showed significantly positive correlations with the levels of CRP,IL-1β, IL-6,TNF-α, lipoprotein(a) [Lp(a)] , serum phosphorus and ages of MHD(P<0.05 or <0.01 ).The levels of intact PTH showed significantly negative correlations with RBW, MAC, MAMC, Alb, Hb and total cholesterol(TC) in MHD patients (P<0.01 or <0.05) . And there was also significantly positive correlation between PTH and MQSGA in MHD patients (P<0.05). Conclusion PTH is probably involved in the presence and the progression of malnutrition-inflammation-atherosclerosis syndrome in MHD patients.

ced glutathione in MHD patients appears to be associated with an improvement of oxidative stress.

Objective To investigate the effect of rosiglitazone on p38 mitogen-activated protein kinase (p38MAPK) pathway in polycystic kidney cyst-lining epithelial cells. Methods The cyst-lining epithelial cells (PKD cells) from human polycystic kidney were treated with rosiglitazone (10 μmol/L), peroxisome proliferator-activated receptor-γ (PPARγ) inhibitor GW9662 (10 μmol/L), rosiglitazone (10 μmol/L) +GW9662 (10 μmol/L), p38MAPK specific inhibitor SB203580 (10 μmol/L), SB203580 (10 μmol/L)+ rosiglitazone(10 μmol/L) for 2 hours followed by epidermal growth factor (EGF) stimulation. Protein expressions of p38, phuspho-p38 (p-p38) and proliferating cell nuclear antigen (PCNA) were detected by Western blot. p38 mRNA was examined by RT-PCR. Expression of c-fos and c-jun was observed by immunocytochemistry. Results (1) EGF markedly up-regulated the expressions of p38, p-p38, PCNA, c-fos anti c-jun compared with control group (P<0.01). (2) Compared with EGF treated group, rosiglitazone significantly reduced p38 activation and mRNA expression (P<0.01, respectively). Rosiglitazone, rosiglitazone+SB203580 could significantly down-regulated p-p38, PCNA, c-fos and c-jun expression (P<0.01, respectively) with no significant difference between these two groups. (3) GW9662 partially reversed the reduction effect of rosiglitazone. Conclusions Rosiglitazone can inhibit proliferation of autosomal dominant polycystic kidney disease cyst-lining epithelial cells partially through down-regulating p38 activation and reducing c-fos, c-jun and PCNA expression. The above effect of rosiglitazone is in part PPARγ-independcnt.