ABSTRACT
Knee osteoarthritis (KOA) is a common chronic degenerative disease of cartilage, which often occurs in middle-aged and elderly patients. It can cause joint swelling, pain and limited movement. With the aging population gradually increasing in China, the prevalence of KOA is also increasing, imposing burdens on patients, families and society. At present, the clinical treatment methods for KOA mainly include physical exercise therapy, non-steroidal analgesic drug therapy, intra-articular hormone injection therapy and surgical treatment, which can improve symptoms and reduce pain but cannot effectively cure KOA. With the development of medicine, platelet-rich plasma (PRP) therapy, as a new treatment method, has the effects of nerve repair and pain relief, and has become a new choice for the treatment of KOA. This article reviews the application of PRP in KOA, so as to provide a new perspective for clinical treatment of knee osteoarthritis KOA.
ABSTRACT
Objective To compare the effect of TNF-α preconditioning and ischemic preconditioning on hepatic ischemia-reperfusion injury ( IRI) and investigate the underlying mechanisms of TNF-αpreconditioning. Methods Fourty healthy male Wistar rats were random-ly divided into four groups which were Sham-operated group ( SO) ,ischemia-reperfusion group ( IR group:produced by total inflow occlusion for 30 min) ,ischemic preconditioning group ( IPC group:induce with 10 min hepatic ischemic and open 10 min before IR) and TNF-αpre-conditioning group ( TPC group:intraperitoneal injection with 1 μg/kg TNF-a 30 min prior to IR) . The sample of blood and hepatic tissue of all groups were taken after experiment. The protein levels of NF-κBp65 and Bcl-2 in the hepatic tissue were detected by immunohistochemis-try. Results There was significant difference (P0. 05) between IPC group and TPC group. Conclusion TNF-α preconditioning decreased the intensity of hepatic IRI,just as ischemic preconditioning,by induces an de-crease in the NF-κBp65 expression and an increase in the Bcl-2 expression.
ABSTRACT
Objective To evaluate the effects of TAT-heme oxygenase-1 (TAT-HO-1) fusion protein on liver injury in rats undergoing orthotopic liver transplantation (OLT).Methods Adult male Lewis (inbred) rats (aged 8-10 weeks,weighing 180-230 g) were used as donors and Brown Norway rats (aged 8-10 weeks,weighing 180-230 g) as recipients.The recipient rats were randomly divided into 2 groups (n=6 each) using a random number table:OLT group and TAT-HO-1 group.The livers were harvested according to the method described by Kamada.In OLT group,the donor livers were flushed and preserved with 4 ℃ HTK solution,while the livers were flushed and preserved for 6 h with 4 ℃ HTK solution containing TAT-HO-1 50 μg/ml in group P.Blood samples were obtained at 7 days after transplantation for measurement of activities of alanine aminotransferase and aspartate aminotransferase in serum.Hepatic specimens were obtained at 7 days after transplantation and stained with haematoxylin and eosin for examination under light microscope.Rejection activity index was calculated according to Banff criteria.The contents of transforming growth factor-beta 1 and interleukin-6 in liver tissues were determined using ELISA.Kupffer cells were isolated and cultured for 48 h to determine the levels of transforming growth factor-beta 1 and interleukin-6 in culture medium.Results Activities of alanine aminotransferase and aspartate aminotransferase in serum,rejection activity index and levels of transforming growth factor-beta 1 and interleukin-6 in liver tissues and culture medium of Kupffer cells were significantly decreased,and the pathological changes of livers were mitigated in group TAT-HO-1 as compared to group OLT.Conclusion TAT-HO-1 fusion protein applied during cold storage of donor livers can attenuate liver injury in rats undergoing OLT.
ABSTRACT
ObjectiveTo investigate effects of anisodamine on myocardial caspase-1 and interleukin-18 expression following overtraining-induced acute myocardial injury in rats.Methods Forty-eight male Wistar rats weighing 200-220 g were randomly divided into 3 groups:group control (group C,n =8) ; group exhausting swim (group ES,n =24) and group anisodamine (group AD,n =16).The animal model of overtraining-induced acute myocardial injury was developed by exhausting swim The animals were forced to swim until they were exhausted.The animals sank to the bottom and no righting reflex or escape response was elicited when they were taken out of water in groups ES and AD.In group AD anisodamine 10 mg/kg was given intraperitoneally 20 min before overtraining.Blood samples were taken from inferior vena cava immediately (T1) and at 6 and 24 h after overtraining (T2,T3 ) in group ES and at T2,T3 in group AD for determination of serum cardiac troponin 1 (cTnI) concentration (by ELISA).The animals were sacrificed after blood sampling and myocardial specimens were obtained for microscopic examination and determination of caspase-1 and interleukin-18 expression (by immuno-histochemistry).ResultsOvertraining significantly increased serum cTnI concentration and up-regulated myocardial caspase-1 and interleukin-18 expression in group ES as compared with group C.Anisodamine significantly attenuated overtraining-induced increase in serum cTnI concentration and myocardial caspase-1 and interleukin-18 expression in group AD as compared with group ES.ConclusionAnisodamine can reduce overtraining-induced acute myocardial injury by down-regulating caspase-1 and interleukin-18 expression.
ABSTRACT
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.
ABSTRACT
Objective To evaluate the role of the expression of heat shock protein 70 (HSP70) and heme oxygenase-1 (HO-1) in the reduction of renal ischemia-reperfusion (I/R) injury by ischemic postconditioning in tats.Methods One hundred and forty healthy male SD rats weighing 250-280 g were randomized into 4 groups ( n = 35 each) : sham operation group (S group) ; I/R group; ischemic postconditioning group (IPo group); quercetin (an inhibitor of HSP) + ischemic postconditioning group (Q + IPo group). Renal I/R was produced by clamping bilateral renal pedicels for 45 min followed by reperfusion. In group S, bilateral kidneys were only exposed through a midline incision but their- pedicels were not clamped. In IPo and Q + IPo groups, 45 min ischemia was followed by three 10 s episodes of ischemia at 10 s intervals for reperfusion and in addition intraperitoneal quercetin 100 mg/kg was injected at 1 h before ischemia in group Q + IPo. Blood samples from hearts were obtained at 0, 1, 3, 6, 12, 24 and 48 h of reperfusion (T0-6) and the rats were then sacrificed and kidneys removed to detect the expression of HSP70 and HO-1 mRNA and protein in renal tissues. The blood samples obtained at T3 were used to determine serum creatinine (Cr) and urea nitrogen (BUN) concentrations and the expression of caspase-3 mRNA . The apoptosis in the renal tissues was detected using TUNEL and apoptotic index ( AI) was calculated. Microscopic examination was performed with light microscope. Results Compared with group S, the serum Cr and BUN concentrations and AI were significantly increased at T3,the expression of caspase-3 mRNA was up-regulated at T3, and the expression of HSP70 and HO-1 mRNA and protein was up-regulated at T0-6 in the other groups (P ＜ 0.05) . Compared with group I/R, the serum Cr and BUN concentrations and AI were significantly decreased at T3, the expression of caspase-3 mRNA was down-regulated at T3, and the expression of HSP70 and HO-1 mRNA and protein was up-regulated at T1-5 in group IPo ( P ＜ 0.05) . Compared with group IPo, the serum Cr and BUN concentrations and AI were significantly increased at T3, the expression of caspase-3 mRNA was up-regulated at T3, and the expression of HSP70 and HO-1 mRNA and protein was down-regulated at T1-5, in group Q + IPo ( P ＜ 0.05) . The microscopic examination showed that the renal I/R injury was significantly attenuated by ischemic postconditioning and the degree of injury in group IPo was similar to that in group I/R. Conclusion The expression of HSP70 and HO-1 is involved in the reduction of renal I/R injury by ischemic postconditioning in rats.
ABSTRACT
Objective To investigate the role of mitochondrial KATP (mito-KATP) channel in reduction of renal ischemia-repeerfusion (I/R) injury by ischemic postconditioning (IPo) in rats. Methods Thirty-five adult male SD rats weighing 250-280 g were randomly divided into 5 groups ( n = 7 each): group Ⅰ sham operation (group S); group Ⅱ I/R; group Ⅲ IPo; group Ⅳ 5-HD + I/R and group V 5-HD + IPo. The rats were anesthetized with intraperitoneal (IP) chloral hydrate 300 mg/kg. Bilateral kidneys were exposed and their pedicles were occluded for 45 min with atraumatic mini-clamp followed by 6 h reperfusion in group Ⅱ - Ⅴ . In group Ⅲ and Ⅴ 3 cycles of 10 s reperfusion followed by 10 s ischemia were applied immediately after 45 min kidney ischemia. In group Ⅳ and Ⅴ 5-HD (a specific blocker of the mito-KATP channel) 10 mg/kg was given IP at 30 min before ischemia. Blood samples were obtained at 6 h of reperfusion for determination of serum creatinine (Cr) and urea nitrogen (BUN) concentrations. The animals were then killed. Bilateral kidneys were removed for determination of mitochondrial membrane potential in the renal tubular epidural cell and intracellular reactive oxygen species (ROS)content and free Ca2+ concentrations. Results Renal I/R significantly increased serum Cr and BUN concentrations and intracellular free Ca2+ concentration and ROC content and decreased mitochondrial membrane potential as compared with sham operation group. IPo significantly attenuated the I/R-induced changes mentioned above. The protective effects of IPo against renal I/R injury was reversed by 5-HD. Conclusion Mito-KATP channel is involved in reduction of I/R-induced renal injury by ischemic postconditioning.
ABSTRACT
Objective To evaluate the role of P2X3 receptors in dorsal root ganglion in development of incisional pain in rats.Methods Twenty-four healthy male SD rats weighing 200-220 g were randomly divided into 3 groups(n = 8 each): control group(group C),incisional pain(group IP)and P2X3 receptor antagonist + IP group(group A).In group IP and A,a 1 cm longitudinal incision was made in the plantar surface of left hindpaw according to the method described by Brennan et al.in isoflurane-anesthetized rats.P2X3 receptor antagonist TNP-ATP 200 nmol was injected into the plantar surface of left hindpaw 30 min after plantar incision was made in group A,while equal volume of normal saline was given instead of TNP-ATP in group C and IP.The behavior of the hindpaw of the rats were assessed using cumulative pain score within 1 h after injection.The animals were sacri ficed 2 h after injection and the dorsal root ganglion was removed for determination of P2X3 receptor expression and intracellular Ca2+ concentrations.ResultsThe cumulative pain scores,P2X3 receptor expression and Ca2 + concentrations were significantly higher in group IP and A than in group C(P ＜ 0.05).The cumulative pain scores,P2X3 receptor expression and Ca2+ concentrations were significantly lower in group A than in group IP(P ＜0.05).Conclusion P2X3 receptors in dorsal root ganglion is involved in the development of incisional pain through increasing intracellular Ca2+ concentrations in rats.