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Objective To investigate the effects of Tim-3 on the renal ischemia-reperfusion injury (IRI),and explore the role of monocyte-macrophage cell system.Methods Totally 72 C57BL/ 6 mice were randomly divided into four groups (n =18 each).(1) IR + Tim-3 rnAb group (experimental group):Each mouse was intraperitoneally injected with 200μg of anti-Tim-3 mAb and the IR model of mouse kidney was established after 1 day;(2) IR + IgG monoclonal antibody group (negative control group):each mouse was intraperitoneally injected with anti-IgG mAb (200 μg) and the IR model of mouse kidney was established after 1 day;(3) IR group:mouse kidney IR model was established only;(4) Control group:mouse kidney IR model was not established.At 6,24 and 48 h after IR respectively,venous blood of 6 mice in each group was taken from the infrarenal vein.Scr and CystinC were detected and PAS staining was used to observe the pathological change of renal tissues.Cell apoptosis was detected by TUNEL staining.Pax,bcl-2 and caspase-3 expression in renal tissue was detected by Western blotting.Immunohistochemistry was used to detect the distribution of Tim-3 and activated macrophage cells.Flow cytometry and ELISA were used to evaluate the level of Tim-3 and inflammatory cytokines secretion respectively.Results Compared with control group,the Tim-3 expression was dramatically increased in IR group and I/R + Tim-3 mAb group.The serum Scr and CystinC levels were increased in IR group,and Tim-3 blocking decreased the levels of serum Scr and CystinC (P＜0.05).PAS and TUNEL staining showed that renal injury score and apoptotic index were higher in IR group than those in control group.Tim-3mAb significantly decreased those markers,and ameliorated the renal tubulointerstitial injury induced by IRk The expression levels of Caspase-3 and Bax/bcl-2 was increased in IR group,but deceased by Tim-3mAb.IR induced F4/80 + distribution and inflammatory cytokines secretion in renal tubular interstitial tissues,while Tim-3mAb down-regulated F4/80 + activation and the levels of inflammatory cytokines.Conclusion The findings demonstrated Tim-3 may promoted renal IRI through regulating mononuclear phagocyte system function.
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Objective To discuss the clinical presentations and imaging features of a novel avianorigin influenza (H7N9).Methods Anteroposterior chest radiographs and serial thin-section CT images in 5 patients with H7N9 were reviewed retrospectively by two radiologists,the predominant inaging patterns of lung abnormalities and clinical data were recorded and analyzed.Results The large consolidation of the right lung with air bronchograms was the most common radiographic appearance in all patients with H7N9 at admission,and the abnormalities were more severe in the bilateral lower lobes.Both lungs developed large,scattered consolidations and ground-glass opacities with the progression of disease.The lesions in the left lung were more rapidly absorbed than those in the right lung.Conclusion Influenza H7N9 has certain chest imaging characteristics in the onset,progression and recovery of disease.
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Objective To observe the month age distribution of peroxisome proliferators activated receptor gamma (PPARγ) expression in rat kedney. Methods Wistar rats aged 3 months,12 months and 24 months were made as models who represented young, middle-aged and old group respectively. Western blotting, immunohistochemical (IHC) and in-situ hybridization (ISH) were used to detect the expression and location of protein and mRNA of PPARγ in rat kidney. Results Western blotting results showed that the expression of PPARγ protein was higher in 3 months group than in 24 months group (0.94±0.05 vs. 0.78±0.02, P＜0.01) and 12 months group (0.87±0.04, P＞0.05), and it reduced in 24 months group than in 12 months group (P＞0.05). By IHC,the PPARγ protein was localized predominantly in the nuclear of tubular epithelia and collecting duct cells in each group. In old age group, PPARγ protein was also detected little in the mesangial and Bowman's capsule epithelial cells. Meanwhile, the distribution of PPARγ mRNA with ISH was consistent with above findings. Additional, semi-quantitative analysis of ISH results verified that the level of PPARγ mRNA decreased with ageing. Conclusions As a nuclear transcription factor,PPARγ participates in the regulation of rat kidney aging.
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Objective To investigate the effect of rosiglitazone (RGTZ) on anti-oxidation in aging rat kidney. Methods Twenty-four-month-old male Sprague-Dawley rats were randomly divided into three groups (n=10): control group (CON), rosiglitazone group (RGTZ) and caloric restriction group (CR). The CON rats were allowed ad libitum access to feed and tap water.The RGTZ rats received intragastric administration of RGTZ (4 mg·kg-1·d-1),and the CR rats were provided with a vitamin and mineral fortified version of the same diet at a level of 40% less food (by weight) than the CON rats. After 12 weeks all the animals were sacrificed by decapitation, and both the body weight and the percentage of kidney and heart in each group were measured.Western blot was performed to analyze the expression of PPARγ protein. The content of MDA and the activity of SOD and GSH-PX in kidney tissue were detected. Besides, frozen sections of kidney tissue were stained for senescence-associated-13 galactosidase (SA-β-Gal). Results The body weight of CR rats decreased obviously, in contrast, which did not change in CON and RGTZ group. Percentage of kidney and heart to body weight was normal in CR or RGTZ group after intervention. Western blot result showed that PPARγ protein expression in rat kidney was significantly higher in RGTZ and CR group as compared to CON group (P<0.05). Compared with RGTZ and CR rats, obviously lower activities of SOD and GSH-Px were noted in CON rats, however, the content of MDA was higher in CON rats. Additionally, the positive staining area of [3-Gal in CR and RGTZ group was significantly smaller than that in CON rats (P<0.05, P<0.01 ). Conclusion RGTZ can defer the kidney aging in senescence SD rat, and the mechanism may be related to amelioration of oxidative damage and enhancement of antioxidation.
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Objective To investigate the role of adhesion molecules P-selectin (CD62P) as a pathogenic factor in Henoch-Schonlein purpura nephritis (HSPN) patients.Methods The expression of adhesion molecules CD62P marked by fluorescent monoclonal antibody in renal biopsy tissue and peripheral blood was studied by flow cytometry in patients with HSPN.The renal tissue was collected and analyzed by light microscopy (HE,PAS,Masson,PASM).Results ① CD62P expressed in renal tissue of 27 cases among all 32 patients with HSPN (84.4%).It expressed mainly in glomerular mesangial area and capillary vessels,then,interstitial small blood vessels,renal tubule.CD62P most significantly expressed in type Ⅲ and Ⅳ,then the type Ⅱ and the last type Ⅰ.② Thirty-two patients of HSPN were highly expressed on CD62P in peripheral blood than those of control group (P