Objective To observe the changes in the expression of renal tissue TNF-α , NF-κB and the interrelation to renal cell apoptosis, and their influences of Inula Britannica(an inhibitor of inflammatory signal pathway) in exhausted swimming rats, and to investigate the role of inflammatory signal pathway. Methods Forty-eight male Wistar rats were randomly divided into three groups: control group (CN, n=8), exhaustive swimming group (ES, n=24) and Inula Britannica group (IB, n=16). The rats of CN were quiet without swimming. The rats of ES swam to exhaustion and were sacrificed at immediately (ESI, n=8), 6 hour (ES 6 h, n=8) and 24 hour (ES 24 h, n=8) after exhanstiing swimming. The rats of IB group took orally Inula Britannica at the dose of 25 ml/kg body weight at 24 h before swimming and then swam to exhaustive state. The rats of IB group were sacrificed at 6 hour (IB 6 h, n=8) and 24 hour (IB 24 h, n=8) after exhaustiing swimming. The renal cell apoptosis was measured by the method of terminal-deoxynucleotidyl transferase mediated d-UTP nick end labeling (TUNEL). The expression of TNF-α in renal tissue was examined by immunohistochemistry. The changes of NF-κB in renal tissue were measured by flow cytometry and immunnhistochemistry. The interrelation between TNF-α and NF-κB was analyzed by Pearson method, and the interrelation between TNF-α, NF-κB and renal tissue cell apoptosis was analyzed by Spearman method. Resulls The number of renal tissue apoptotic cells was increased progressively from ESI to ES 24 h rats (P <0.05). Immunohistochemistry staining showed that the positive expressions of renal tissue TNF-α and NF-κB were increased progressively at 0 h (0.136±0.009, 0.129±0.011), 6 h (0.171±0.011, 0.166± 0.009) and 24 h (0.229±0.008, 0.218±0.019) after exhaustiing swimming in ES compared with control group (0.109±0.010, 0.095±0.010) ( all P<0.05). The similar changes of renal tissue NF-κB was also revcalved by flow cytometry. The expression of TNF-α was positively correldted with NF-κB (r=0.955, P<0.01 ), and renal cell apoptosis was also positively correlated with TNF-α and NF-κB (r =0.953, r=0.939, P<0.01) in ES rats. Pretreatment with Inula Britannica, inhibited the up-regulation of expressions of renal tissue TNF-α (6 h:0.142±0.012, 24 h:0.130±0.010) and NF-κB (6 h:0.138±0.010, 24 h:0.136±0.011 ) induced by exhausting swimming. Conclusion Overtraining can induce the up-regulating expressions of renal tissue TNF-α and NF-κB, and Inula Britannica can partly counter the above changes in exhaustied swimming rats, which may be one important mechanisms of overtraining-induced renal tissue cell apoptosis and the anti- apoptosis effect of Inula Britannica.

Objective To study the expressions of apoptosis related genes Bcl-2 and Bax proteins in rat's renal tissue and the relationship between the ratio of Bcl-2/Bax and renal cell apoptosis induced by overtraining,and observe the effect of anisodamine on the expression of genes Bcl-2 and Bax in exhausted rats.Methods The animal model of acute kidney injury induced by exhausting swimming was reproduced.Forty eight male Wistar rats were randomly assigned into sedentary control group(CN,n=8),exhausting swimming group(immediate,6 hours and 24 hours after exhausting swimming,ESI,ES6h and ES24h,8 each),Anisodamine group(6 hours and 24 hours after exhausting swimming,AD6h and AD24h,8 each).The expressions of Bcl-2 and Bax were detected by immunohistochemical staining and image analyzer.The correlation between the ratio of Bcl-2/Bax and renal cell apoptosis was analyzed.Results The analysis showed that the expression of Bax increased,and of Bcl-2 decreased,the ratio of Bax/Bcl-2 increased remarkably in ESI group compared with CN group(P

Objective To observe the expression changes of renal tissue Bax,Bcl-2 and caspase-3,to wxamine the correlation between the ratio of Bax to Bcl-2,caspase-3 and renal tubular cells apoptosis,and to investigate the role of caspase-related signal pathway.Methods Forty-eight male Wistar rats were randomly divided into three groups: control (CN,n=8),exhaustive swimming (ES,n=24) and inula britannica (IB,n=16) group.The rats of CN were quiet without swimming.The rats of ES swam to exhaustive state and were sacrificed at immediately(ESI),6 hour (ES 6 h) and 24 hour (ES 24 h) after exhaustive swimming respectively.The rats of IB took orally inala britannica at the dose of 25 ml/kg body weight at 24 h before swimming and then swam to exhaustive state.The rats of IB group were sacrificed at 6 hour (IB 6 h) and 24 hour (IB 24 h)after exhaustive swimming.The animal model of overtraining-induced acute kidney injury was developed by exhaustive swimming.The renal cell apoptosis was measured by the method of TUNEL.The expressions of Bax,Bcl-2,caspase-3 in renal tissue were observed by immunohistochemistry.The expression of caspase-3 protein was examined by Western blotting.The correlation between the ratio of Bax to Bcl-2 and caspase-3 was analysed by Pearson method,and the correlation between the ratio of Bax to Bcl-2,caspase-3 and renal tubular cell apoptosis was analysed by Spearman method.Results The number of renal tubular apeptotic cells was increased progressively in ESI to ES 24 h rats by TUNEL (P＜0.05).Immunohistochemistry staining showed that the ratio of Bax to Bcl-2 and caspase-3 in renal tubular cells were increased progressively at 0 h,6 h and 24 h after exhaustive swimming compared with control group (P＜0.05).The change of renal tissue caspase-3 was also revealved by Western blotting analysis.The ratio of Bax to Bcl-2 and caspase-3 in renal tubular cell was correlated positively (r=0.865,P＜0.05),The ratio of Bax to Bcl-2,and caspase-3 was also correlated positively to renal tubular cell apoptosis (r=0.674,r=0.837,P＜0.05) in ES rats.Pretreatment with inula britannica inhibited the up-regulation of the ratio of Bax to Bcl-2,caspase-3 and cell apoptosis in renal tubular cell induced by exhaustive swimming.Conclusion Overtraining can induce renal tubular cells apoptosis through activating caspase-related signal pathway by impairing the balance of Bax and Bcl-2,which may be one of the important molecular mechanisms of overtraining-induceed renal tubular cells apoptosis.

Objective To investigate the clinical effects of fenofibrate and polyene phosphatidylcholine in treatment of non-alcoholic fatty liver disease.Methods 86 patients with non-alcoholic fatty liver disease were randomly divided into two groups.45 cases in therapy group received 0.2g of fenofibrate once a day,and the others in control group received 456mg of polyene phosphatidylcholine for three times per day.All of the patients were treated for 12 weeks.Liver function,blood fat,clinical effect and liver B ultrasonic were analyzed before treatment and after 12 weeks.Results The improvement of liver function,blood fat,and liver ultrasonic imaging in therapy group was better than that in the control group.The cure rate was 82.2％ in therapy group and 63.4％ in control group.There was a statistical significance between the two groups ( x2 =3.874,P ＜ 0.05).Conclusion Fenofibrate had significant therapeutic effect in treatment of non-alcoholic fatty liver disease with lower costs and lower side effects.

Objective To investigate the renal histopathological changes of over training induced acute renal injury in human being.Methods Eight patients treated in our hospital admitted overtraining were observed retrospectively about their clinical and pathological data,including clinical features,laboratory tests and pathological examinations.Results Eight patients with acute kidney injury after overtraining,manifested as urine occult blood positive in 2 cases,3 cases of urinary protein,urinary occult blood and urine protein were positive in 3 cases.Five cases of renal dysfunction,manifested as creatinine,urea nitrogen,uric acid significantly increased; renal ultrasound non-specific changes,manifested as increased echogenicity of the cortex.2 cases of renal pathology glomerular ischemic; Two cases of renal interstitial mild edema,five cases of inflammatory cell infiltration; Three cases of renal tubular epithelial vacuolar degeneration,2 cases of tubular atrophy,4 cases of renal tubular epithelial brush border loss,see intraluminal protein casts can be seen,1 case of calcium deposition.Conclusion The acute renal injury can be induced by overtraining.Kidney pathology ischemic is the most important change and renal tubular show most sensitive features of ischemic.In addition,inflammatory response and striated muscle damage were also induced because of overtraining.

Objective To evaluate the effects of anisodamine on apoptosis in cardiomyocytes and inflammatory response in overtrained rats. Methods Twenty-four male Wistar rats, weighing 200-220 g, were randomly divided into 3 groups ( n = 8 each) : control group (group C) , overtraining group (group O) , anisodamine group (group A) . The model of overtraining-induced acute heart injury was established by exhausting swimming. Anisodamine 10 mg/kg was given intraperitoneally 20 min before overtraining in group A. Blood samples were taken at 6 h after overtraining for measurement of serum CK-MB activity. The rats were then sacrificed and myocardial tissues taken for determination of TNF-α content and NF-κB activity (by immunohistochemistry) . The apoptosis rate was detected by flow cytometry. Results The CK-MB activity, apoptosis rate, TNF-α content and NF-κB activity were significantly higher at 6 h after overtraining in groups O and A than in group C, while lower at 6 h after overtraining in group A than in group O ( P < 0.05) . Conclusion Anisodamine can inhibit apoptosis in cardiomyocytes by reducing inflammatory response in overtrained rats.

Objective To study the role of endothelin-1 (ET-1) and angiotensin Ⅱ (AngⅡ) in over-exertion induced acute kidney injury (OTIAKI) by observing the changes in ET-1 and AngⅡ contents in plasma and renal tissue and their relationship with OTIAKI in exhausted rats. Methods 40 male Wistar rats were randomly divided into two groups: control group (CN, n=8) and exhaustion group (ES, n=32). The exhaustion group, depending on the recovery time after exhaustion, was further divided into 4 subgroups (8 each): immediate subgroup (ESI), 6h after exhaustion subgroup (ES 6h), 12h after exhaustion subgroup (ES 12h) and 24h after exhaustion subgroup (ES 24h). The animal model of OTIAKI was reproduced by exhausting swimming, while the rats in control group were not forced to swim. The contents of serum urea (Ur) and creatinine (Cr) in each group were serially measured. The renal specimens were observed with a light microscope to study their morphologic changes. Renal cell apoptosis was detected using terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) assay. The contents of ET-1 and AngⅡ in plasma and renal tissue were measured by radio-immunoassay (RIA). The correlation between the content of ET-1 and the levels of serum Ur and Cr were was analyzed by Pearson method, and the correlation between the content of AngⅡ in renal tissue and cell apoptosis was analyzed by Spearman method. Results The levels of serum Ur and Cr were significantly increased in ESI group (P

Objective To investigate the relationship between hepatitis B virus reactivation and the level of blood T-lymphocyte subsets.Methods T lymphocyte subsets ( CD3,CD4,CDs ),CD4/CDs level of 40 patients with chronic carriers of hepatitis B virus and 35 patients with hepatitis B virus re-activation were detected by Flow cytometry(Epics XL).Results The hepatitis B virus reactivation in patients with CD3,CD4 and CD4/CDs levels were significantly lower than the chronic hepatitis B virus carriers,The difference between the two groups patients was significant[(71.31 ±5.20)％ vs (68.57 ±6.10)％,(37.82 ±4.90)％ vs (32.12 ±5.93)％,(1.37 ±0.28) vs (1.18 ±0.43 ),all P ＜ 0.05].Conclusion The levels of CD3,CD4 and CD4/CD8 ratio were significantly declined,it may be the one important reason of hepatitis B virus reactivation.

Objective To investigate the effects of valsartan on the expression of connective tissue growth factor(CTGF) in rat glomerular mesangial cells incubated with high concentration of glucose.Methods We used high concentration glucose and valsartan to stimulate the cultured rat glomerular mesangial cells in vitro. The protein expressions of CTGF and the activation of P38 mitogen-activated protein kinase(P38 MAPK) and cAMP response element binding protein 1(CREB1) were tested by Western blot. CTGF and fibronectin(FN) mRNA were measured by reverse transcription and polymerase chain reaction (RT-PCR). The protein synthesis of lamanin (LN) and type IV collagen in the supernatants of the GMCs were detected by radioimmunoassay. Results Compared with low glucose control group,the expression of CTGF,p-P38 MAPK,p-CREB1,CTGF mRNA,FN mRNA,LN and type IV collagen in the supernatants were significantly increased in GMCs incubated with high concentration of glucose medium. The expression levels of CTGF,p-P38 MAPK,p-CREB1,CTGF mRNA and FN mRNA were significantlylower in the valsartan group than those in the high concentration glucose group. The concentrations of LN and type IV collagen in the supernatantsin the valsartan group were also lower than those in the high concentration glucose group. Conclusion Valsartan can inhibit expression of CTGF and ECM proteins in rat glomerular mesangial cells incubated with high concentration of glucose,partly by regulating the phosphorylation of P38 MAPK and CREB1.

Objective To evaluate the effect of penehyclidine hydrochloride pretreatment on rhabdomyolysis-induced acute kidney injury (AKI) in rats.Methods Forty-two pathogen-free male SpragueDawley rats,weighing 200-220 g,aged 2 months,were randomly divided into 3 groups using a random number table:control group (group C,n =6),AKI group (n =18),and penehyclidine hydrochloride group (group PH,n =18).The model of rhabdomyolysis-induced AKI was established by injecting 50％ glycerol 10 ml/kg into the lateral muscle of bilateral hindlimbs in AKI and PH groups.The equal volume of normal saline was given in group C.Penehyclidine hydrochloride 0.2 mg/kg was injected intraperitoneally at 30 min before administration of glycerol in group PH.Six rats were selected at 1 h after administration of normal saline in group C,or at 1,6 and 24 h after administration of glycerol,blood samples were collected from the inferior vena cava for determination of the serum blood urea nitrogen (BUN) and creatinine (Cr) concentrations by enzymic colorimetric method.The animals were sacrificed,and kidney specimens were obtained for pathologic examination and for determination of the expression of DJ-1 and phosphatase tensin homolog deleted on chromosome 10 (PTEN) encoding protein (by immuno-histochemistry and Western blot).The damage to the renal tubules was scored.Results Compared with group C,the serum BUN and Cr concentrations and renal tubular damage score were significantly increased,the expression of D J-1 was down-regulated,and the expression of PTEN protein was up-regulated in group AKI (P＜0.05 or 0.01).Compared with group AKI,the serum BUN and Cr concentrations and renal tubular damage score were significantly decreased,the expression of DJ-1 was up-regulated,and the expression of PTEN protein was down-regulated in group PH (P＜0.05 or 0.01).Conclusion Penehyclidine hydrochloride pretreatment can reduce rhabdomyolysis-induced AKI probably by up-regulating the expression of DJ-1 and down-regulating the expression of PTEN protein in rats.