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 evaluate the effect of anisodamine on expression of Toll-like receptor 4 (TLR4) in the kidneys of exhausted rats.Methods Forty-eight male SD rats weighing 200-220 g were randomly divided into 3 groups:control group (group Ⅰ ) (.n =8) ; exhaustion group (group Ⅱ ) ( n =24) and anisodamine group (gronp Ⅲ) (n =16).In groups Ⅱ and Ⅲ exhaustion was induced by exhausting swimming and defined by (1) the animal sank to the bottom and stayed for＞ 10 s during swimming,(2) uncoordinated swimming,and (3) the animal lost escape/righting reflex when placed on the table In group Ⅲ intraperitoneal anisodamine 10 mg/kg was administered at 20 min before swimming.The animals were sacrificed immediately (T1 ),6 h (T2 ) and 24 h (T3 ) after exhaustion respectively.Their kidneys were obtained for detection of apoptosis and determination of TLR4 protein (by immuno-histochemical staining) and mRNA (by RT-PCR).Results Exhaustion significantly increased the number of apoptotic cells and up-regulated TLR4 protein and mRNA expression in group Ⅱ as compared with group Ⅰ,and anisodamine significantly attenuated the exhaustion-induced increase in the number of apoptotic cells and up-regulation of TLR4 protein and mRNA expression in group Ⅲ as compared with group Ⅱ.Conclusion Anisodamine can decrease apoptosis in renal cells in exhausted rats bydown-regulating TLR4 expression.

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 study the cardiomyocyte and renal cell apoptosis induced by overtraining, and the preventive effects of anisodamine against the adverse effects. Methods The rats were forced to swim till exhaustion to reproduce the animal model of overtraining. The animals were randomly divided into control group, exhausted group and anisodamine group. The exhausted group, depending on the recovery time after exhaustion, was divided again into exhaustion subgroup, 6h after exhaustion subgroup, and 24h after exhaustion subgroup. The animals in the anisodamine group received intraperitoneally 10mg/kg of anisodamine before the swimming overtraining, and divided again into 6h after anisodamine injection subgroup and 24h anisodamine injection subgroup. The cardiomyocyte and renal cell apoptosis was observed by the method of TUNEL, image analysis and flow cytometry. Results It was revealed by TUNEL that the number of apoptotic cardiomyocytes was increased after exhaustive swimming, especially in the 6h after exhaustion subgroup. The number of apoptotic cells was also increased in kidney of 0h, 6h and 24h after exhaustion subgroups, especially in 24h after exhaustion subgroup. The apoptosis ratio was also increased significantly in 0h, 6h and 24h after exhaustion subgroups as demonstrated by flow cytometry. Compared with the rats of exhausted group, the number of apoptotic cells in heart and renal tissue was decreased remarkably after anisodamine injection. Conclusion The apoptosis of cardiomyocyte and renal cell could be induced by exhaustive swimming. Compared with kidney, heart injury recovered more quickly. Anisodamine had the preventive effect on the injury to heart and kidney in exhausted rats.

Objective:To investigate the clinical efficacy and safety of biopolysaccharide colloidal solution (Shutaishu) in the prevention of intestinal adhesion after abdominal surgery.Methods:A total of 100 patients scheduled to undergo abdominal surgery in Quzhou Municipal Hospital of Traditional Chinese Medicine from February to October in 2019 were included in this study. They were randomly divided into an observation group and a control group, with 50 patients in each group. Before closing the abdomen after surgery, abdominal cavity and wound were flashed with Shutaishu and 0.9% sodium chloride injection in the observation and control groups, respectively. The recovery of gastrointestinal function, intestinal adhesion, abdominal pain and the incidence of complications were compared between the observation and control groups.Results:The time to first regular bowel sound [(28.81 ± 5.56) h], time to first passage of flatus [(36.34 ± 6.24) h], time to first defecation [(41.65 ± 8.77) h], time taken for walking [(3.78 ± 0.64) d] in the observation group were significantly shorter than those in the control group [(32.75 ± 5.15) h, (41.51 ± 6.84) h, (48.05 ± 9.81) h, (4.27 ± 0.69) d, t = 3.68, 3.95, 3.89, 3.68, all P < 0.001]. At 5 and 30 days after surgery, the incidence of intestinal adhesion in the observation group [10.0% (5/50), 12.0% (6/50)] was significantly lower than that in the control group [26.0% (13/50), 30.0% (15/50), χ2 = 4.34, 4.88, both P < 0.05]. The total incidence of postoperative complications in the observation group was significantly lower than that in the control group [26.0% (13/50) vs. 54.0% (27/50), χ2 = 8.17, P < 0.05]. With time, visual analogue scale score was significantly decreased in both groups ( t = 3.51, 6.18, both P < 0.05). At 1, 3 and 5 days after surgery, visual analogue scale score in the observation group was significantly lower than that in the control group ( t = 4.07, 4.95 and 8.02, all P < 0.05). Conclusion:Biopolysaccharide colloidal solution is of high clinical value in the prevention of intestinal adhesion after abdominal surgery because it can promote the recovery of gastrointestinal function and early functional exercise, and has no obvious adverse reactions and complications.

Objective To investigate the effect of penehyclidine hydrochloride ( PHC) pretreat?ment on nuclear factor erythroid 2?related factor 2∕heme oxygenase?1 ( Nrf2∕HO?1) signaling pathway in re?nal tissues of rats with rhabdomyolysis?induced acute kidney injury ( AKI) . Methods Thirty?six pathogen?free male Sprague?Dawley rats, weighing 200-220 g, were assigned into 3 groups ( n=12 each) using a random number table: control group (group C), group AKI and PHC pretreatment group (group PHC). Rhabdomyolysis was induced by intramuscular injection of 50% glycerol 10 ml∕kg in bilateral hindlimbs. PHC 0?2 mg∕kg was injected intraperitoneally at 30 min before glycerol was injected intramuscularly in group PHC. At 1 and 6 h after glycerol injection, serum was collected for determination of blood urea nitro?gen ( BUN) and creatinine ( Cr) concentrations, and bilateral kidneys were harvested for pathological ex?amination and for determination of HO?1 activity and expression of Nrf2 mRNA and HO?1 mRNA ( by quan?titative real?time polymerase chain reaction) , Nrf2 in nucleoprotein and total protein and HO?1 in total pro?tein in renal tissues ( by Western blot) . The damage to the renal tubules was scored. Results Compared with group C, the BUN and Cr concentrations in serum and renal tubular damage scores were significantly increased, the expression of Nrf2 in nucleoprotein and total protein and HO?1 in total protein was signifi?cantly up?regulated, and HO?1 activity was significantly increased in AKI and PHC groups, the expression of HO?1 mRNA was significantly up?regulated in group AKI, and the expression of Nrf2 mRNA and HO?1 mRNA was significantly up?regulated in group PHC (P<0?01 or 0?05). Compared with group AKI, the BUN and Cr concentrations in serum and renal tubular damage scores were significantly decreased, the ex?pression of Nrf2 in nucleoprotein and total protein and HO?1 in total protein was significantly up?regulated, and HO?1 activity was significantly increased in group PHC ( P<0?01 or 0?05) . Conclusion The mecha?nism by which PHC pretreatment attenuates rhabdomyolysis?induced AKI may be related to activation of Nrf2∕HO?1 signaling pathway in renal tissues of rats.

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 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.