0.05).Conclusion Tripterygium wilfordii,combined with routine treatment,appeared to decrease 24-hour proteinuria in a certain extent and did not adversely affect liver function,renal function and the blood routine test in most patients with diabetic nephropathy.

Objective:To evaluate the role of Jumonji domain-containing 3 (JMJD3) in cisplatin-induced renal fibrosis following acute kidney injury in mice.Methods:Forty-eight healthy C57BL/6 male mice, aged 8-10 weeks, weighing 20-30 g, were divided into 4 groups ( n=12 each) using a random number table method: control group (group CON), control plus JMJD3 inhibitor group (group CON-A), cisplatin group (group CIS), and cisplatin plus JMJD3 inhibitor group (group CIS-A). In group CIS and group CIS-A, cisplatin was intraperitoneally administered on 1st and 14th days, respectively, to develop a renal fibrosis model in mice with acute kidney injury, and the JMJD3 inhibitor GSKJ4 10 mg/kg and equal volume of PBS were intraperitoneally injected on 4th day, respectively, once every 3 days, 6 injections in total.The equal volume of PBS and GSKJ4 10 mg/kg were intraperitoneally injected at the corresponding time points in group CON and group CON-A, respectively.Six mice in each group were selected, and orbital blood samples were collected on 3rd day after the first injection of cisplatin to determine the concentrations of serum creatinine (Cr) and blood urea nitrogen (BUN), then the animals were sacrificed, and kidney tissues were obtained for microscopic examination of pathological changes after HE and PAS staining (with a light microscope), and the damage to kidneys was assessed and scored.Six mice were sacrificed on 28th day after the first injection of cisplatin, and kidney tissues were removed for determination of the area of renal fibrosis ( via Sirius red and Masson staining), expression of fibronectin (Fn), collagen type Ⅰ (Col Ⅰ) and α-smooth muscle actin (α-SMA) (by immunofluorescence), F4/80 + cell and CD3 + cell count (using immunohistochemical method), and expression of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), CXC chemokine ligand 16 (CXCL16), and monocyte chemoattractant protein1 (MCP-1) mRNA (by real-time polymerase chain reaction). Results:Compared with group CON, the serum BUN and Cr concentrations, renal injury scores, and area of renal fibrosis were significantly increased, the expression of Fn, Col Ⅰ and α-SMA was up-regulated, the F4/80 + cell and CD3 + cell count was increased, and the expression of IL-6, CXCL16, TNF-α and MCP-1 mRNA was up-regulated in group CIS ( P<0.05), and no significant change was found in the parameters mentioned above in group CON-A ( P>0.05). Compared with group CON-A, the serum BUN and Cr concentrations, renal injury scores, and area of renal fibrosis were significantly increased, the expression of Fn, Col Ⅰ and α-SMA was up-regulated, the F4/80 + cell and CD3 + cell count was increased, and the expression of IL-6, CXCL16, TNF-α and MCP-1 mRNA was up-regulated in group CIS-A ( P<0.05). Compared with group CIS, the serum BUN and Cr concentrations, renal injury scores, and area of renal fibrosis were significantly decreased, the expression of Fn, Col Ⅰ and α-SMA was down-regulated, the F4/80 + cell and CD3 + cell count was decreased, and the expression of IL-6, CXCL16, TNF-α and MCP-1 mRNA was down-regulated in group CIS-A ( P<0.05). Conclusions:JMJD3 is involved in the process of renal fibrosis following acute kidney injury in mice, and the mechanism may be related to promotion of inflammatory responses.

Objective:To evaluate the role of histone demethylase (JMJD3) in drug-induced acute kidney injury (AKI) in mice.Methods:Twenty-four male C57BL/6 mice, aged 8-10 weeks, weighing 20-30 g, were divided into 4 groups ( n =6 each) using a random number table method: control group (C group), AKI group, a specific JMJD3 inhibitor GSKJ4+ control group (GSKJ4 group), and GSKJ4-AKI group.Folic acid 250 mg/kg was injected intraperitoneally to develop AKI model.GSKJ4 20 mg/kg was intraperitoneally injected at 1 h before developing AKI model in GSKJ4-AKI group and at the corresponding time point in GSKJ4 group.Blood samples were collected at 72 h after development of AKI model for determination of serum BUN and Cr concentrations.The animals were then sacrificed and renal tissues were collected for microscopic examination of histopathological morphology (using HE and PAS staining) and for determination of cell apoptosis (by TUNEL) and expression of JMJD3, Bax and cleaved caspase-3 (by Western blot), the number of JMJD3, myeloperoxidase (MPO), F4/80 and CD3 positive cells, expression of cleaved caspase-3 and Bax, and expression of IL-1β, IL-6, TNF-α and monocyte chemotactic protein 1 (MCP-1) mRNA (by reverse transcription polymerase chain reaction). The damage to the renal tubules was scored. Results:Compared with C group, the serum BUN and Cr concentrations and renal tubular damage score were significantly increased, the number of JMJD3, myeloperoxidase (MPO), F4/80 and CD3 + positive cells was increased, the number of apoptotic cells was increased, and the expression of Bax, cleaved caspase-3, JMJD3 and IL-1β, TNF-α, IL-6 and MCP-1 mRNA was up-regulated in AKI group ( P<0.05), and no significant change was found in the parameters mentioned above in GSKJ4 group ( P>0.05). Compared with AKI group, the serum BUN and Cr concentrations and renal tubular damage score were significantly decreased, the number of JMJD3, myeloperoxidase (MPO), F4/80 and CD3 positive cells was decreased, the number of apoptotic cells was decreased, and the expression of Bax, cleaved caspase-3, JMJD3, and IL-1β, TNF-α, IL-6 and MCP-1 mRNA was down-regulated in GSKJ4-AKI group ( P<0.05). Conclusions:The mechanism of drug-associated AKI may be related to up-regulation of JMJD3 expression and thus induces cell apoptosis and inflammatory responses in mice.

OBJECTIVE To explore the protective effects and potential mechanisms of Hirudo on mice with non-alcoholic fatty liver disease （NAFLD） in mice. METHODS The male ApoE－/－ mice were randomly divided into the model group and Hirudo low- dose and high-dose groups （0.45， 0.9 g/kg）， with 10 mice in each group； another 10 wild-type male C57BL/6J mice were chosen as the control group. The control group was fed with basal maintenance chow and the remaining groups were fed with high-fat chow for 12 weeks to establish the NAFLD model. Each administration group was given corresponding solution intragastrically， once a day， for 8 consecutive weeks. In the 13th week， the body weight and liver weight of mice in each group were measured after the last medication， and the liver index was calculated； the serum levels of nuclear factor-κB （NF-κB）， tumor necrosis factor-α （TNF- α）， interleukin-1β （IL-1β）， IL-6， total cholesterol （TC）， triglyceride （TG）， low-density lipoprotein cholesterol （LDL-C） and high-density lipoprotein cholesterol （HDL-C） were detected； the liver pathomorphological changes were observed； the protein expressions of peroxisome proliferator-activated receptor γ（PPARγ） and silence information regulator type 1 （SIRT1） were detected. RESULTS Compared with the control group， the liver tissue of mice in the model group showed more fat vacuoles and infiltration of inflammatory cells， with significant lipid accumulation； the body weight， liver weight and liver index of the mice， and serum levels of NF-κB， TNF-α， IL-1β， IL-6， TC， TG and LDL-C significantly increased， while the serum level of HDL-C， the protein expressions of PPARγ and SIRT1 in liver tissues significantly decreased （P＜0.01）. Compared with the model group， the pathological changes in liver tissue of mice were all relieved in Hirudo low-dose and high-dose groups； the body weight， liver weight and liver index， the serum levels of NF-κB， TNF-α， IL-1β， IL-6， TC， TG and LDL-C decreased significantly， while the serum level of HDL-C， the protein expressions of PPARγ and SIRT1 in liver tissue all increased significantly （P＜0.05 or P＜0.01）. CONCLUSIONS Hirudo can regulate liver lipid metabolism and inhibit inflammation by activating the protein expressions of PPARγ and SIRT1， thus having a significant ameliorative effect on NAFLD.