Role of blood markers in predicting the failure of prosthesis removal and antibiotic-loaded bone cement spacer implantation for treatment of periprosthetic joint infection / 中华外科杂志

Objective: To investigate the value of inflammation,coagulation and nutrition markers in predicting the failure of prosthesis removal and antibiotic-loaded bone cement spacer implantation for treatment of periprosthetic joint infection(PJI). Methods: A retrospective study was conducted on 70 patients who undertook prosthesis removal and antibiotic-loaded bone cement spacer implantation due to PJI from June 2016 to October 2020 in the Department of Orthopedics,Henan Provincial People's Hospital. There were 28 males and 42 females,aged (65.5±11.9) years (range: 37 to 88 years). Patients were divided into two groups as the successful group and the failed group depended on whether reinfection occurred after prosthesis removal and antibiotic-loaded bone cement spacer implantation at the last follow up. Patient demographics,laboratory values (C-reactive protein (CRP),erythrocyte sedimentation rate (ESR),ESR and CRP ratio (ESR/CRP),white blood cell count(WBC),platelet count(PLT),hemoglobin(HB),total lymphocyte count(TLC),albumin、fibrinogen(FIB),CRP and albumin ratio (CAR),prognostic nutritional index(PNI)),and reinfection rates were assessed. Comparison between groups was conducted by the independent sample t test or χ2 test. Receiver operating characteristic (ROC) curve was plotted,and the area under the curve (AUC),optimal diagnostic threshold,sensitivity,and specificity were analyzed to predict the failure of prosthesis removal and antibiotic-loaded bone cement spacer implantation. Results: All patients were followed up for at least two years,and the follow-up time was (38.4±15.2) months (range: 24 to 66 months). Fifteen patients suffered failure after prosthesis removal and antibiotic-loaded bone cement spacer implantation,while the other 55 patients succeeded. The overall failure rate of prosthesis removal and antibiotic-loaded bone cement spacer implantation in PJI treatment was 21.4%. Level of preoperative CRP(35.9±16.2)mg/L,PLT(280.0±104.0)×109/L and CAR 1.3±0.8 in successful group were lower than CRP (71.7±47.3)mg/L,PLT (364.7±119.3)×109/L and CAR 2.5±2.0 in failed group (all P<0.05).Whereas,level of preoperative ESR/CRP (3.3±3.1), Albumin (35.3±5.2)g/L and PNI 43.6±6.2 in successful group were higher than ESR/CRP (1.6±1.4),Albumin(31.3±4.8)g/L and PNI (39.2±15.1) in failed group (all P<0.05). AUC of ROC curve,optimal threshold value,sensitivity and specificity of CRP,ESR/CRP, PLT, Albumin,CAR and PNI for the predicting failure of prosthesis removal and antibiotic-loaded bone cement spacer implantation were 0.776(95%CI:0.660 to 0.867),35.4 mg/L,86.7%,67.3%;0.725(95%CI:0.605 to 0.825),1.0,60.0%,78.2%;0.713(95%CI:0.593 to 0.815),253,93.3%,47.3%;0.721(95%CI:0.601 to 0.822),35.7,93.3%,49.1%;0.772(95%CI:0.656 to 0.863),1.1,86.7%,67.3%;0.706(95%CI:0.585 to 0.809),45.7,100%,41.8% respectively. Conclusion: In patients with PJI,CRP>35.4,ESR/CRP≤1.0 and CAR>1.1 could predict the failure of prosthesis removal and antibiotic-loaded bone cement spacer implantation.

The effect of regions-of-interest and elasticity modulus selection on differentiating benign and malignant cervical lymph nodes with shear wave elastography

OBJECTIVE: Imaging diagnosis of cervical lymphadenopathy has conventionally used ultrasonography. Shear wave elastography (SWE) is a recent ultrasound technological advancement that has shown promise in the important medical problem of differentiating between benign and malignant cervical lymph nodes based on quantitative measurements of elasticity modulus. However, widely varying elasticity modulus metrics and regions-of-interest (ROIs) were used in existing studies, leading to inconsistent findings and results that are hard to compare with each other. METHODS: Using a large dataset of 264 cervical lymph nodes from 200 patients, we designed a study comparing three elasticity modulus metrics (Emax, Emean, and standard deviation-SD) with three different ROIs to evaluate the effect of such selections. The metric values were compared between the benign and malignant node groups. The different ROI and metric selections were also compared through receiver operating characteristics curve analysis. RESULTS: For all ROIs, all metric values were significantly different between the two groups, indicting their diagnostic potential. This was confirmed by the ≥0.80 area under the curve (AUC) values achieved with these metrics. Different ROIs had no effect on Emax, whereas all ROIs achieved high performance at 0.88 AUC. For Emean, the smallest ROI focusing on the area of the highest elasticity achieved the best diagnostic performance. In contrast, the larger ROIs achieved higher performances for SD. CONCLUSIONS: This study illustrated the effect of elasticity modulus and ROI selection on the diagnostic performance of SWE on cervical lymphadenopathy. These new findings help guide relevant future studies and clinical applications of this important quantitative imaging modality.

Involvement of endothelial CK2 in the radiation induced perivascular resistant niche (PVRN) and the induction of radioresistance for non-small cell lung cancer (NSCLC) cells

BACKGROUND: Tumor microenvironment (TME) plays a vital role in determining the outcomes of radiotherapy. As an important component of TME, vascular endothelial cells are involved in the perivascular resistance niche (PVRN), which is formed by inflammation or cytokine production induced by ionizing radiation (IR). Protein kinase CK2 is a constitutively active serine/threonine kinase which plays a vital role in cell proliferation and inflammation. In this study, we investigated the potential role of CK2 in PVRN after IR exposure. RESULT: Specific CK2 inhibitors, Quinalizarin and CX-4945, were employed to effectively suppressed the kinase activity of CK2 in human umbilical vein endothelial cells (HUVECs) without affecting their viability. Results showing that conditioned medium from IR-exposed HUVECs increased cell viability of A549 and H460 cells, and the pretreatment of CK2 inhibitors slowed down such increment. The secretion of IL-8 and IL-6 in HUVECs was induced after exposure with IR, but significantly inhibited by the addition of CK2 inhibitors. Furthermore, IR exposure elevated the nuclear phosphorylated factor-κB (NF-κB) p65 expression in HUVECs, which was a master factor regulating cytokine production. But when pretreated with CK2 inhibitors, such elevation was significantly suppressed. CONCLUSION: This study indicated that protein kinase CK2 is involved in the key process of the IR induced perivascular resistant niche, namely cytokine production, by endothelial cells, which finally led to radioresistance of non-small cell lung cancer cells. Thus, the inhibition of CK2 may be a promising way to improve the outcomes of radiation in nonsmall cell lung cancer cells.

Correlation of advanced glycation end products to Alzheimer's disease / 解放军医学杂志

Alzheimer's disease (AD) is a common retrograde neurodegenerative disease of the central nervous system,as well as the most common type of dementia in the aged,the main manifestations of AD are progressive decline of cognitive function and daily life ability.AD seriously affects the quality of life and physical and mental health of the aged,and increased the burden of family and society.The etiology and pathogenesis of AD remain unclear nowadays,and there is no objective and specific biological marker to help the early diagnosis and effective treatment.Advanced glycation end products (AGEs) are stable end products formed by non enzymatic reaction between the free amino groups of proteins,lipids,nucleic acids macromolecules and the carbonyls of glucose or other reduced sugars.Recent years,more and more studies have focused on the correlation between AGEs and its receptors (RAGE) in patients with cognitive impairment,however,the role played by AGEs in the pathogenesis of AD remains unclear.The present paper will give an overview from three aspects:the structure and characteristics of AGEs,the relationship between the occurrence and development of AD and AGEs and the relationship between AGEs and prognosis of cognitive impairment which we've known so

Anti-oxidation and anti-apoptosis mechanism of Xinshao formula on cerebral ischemia reperfusion injury / 中国中药杂志

The cerebral ischemia-reperfusion model was established to investigate the anti-oxidation and anti-apoptosis mechanism of Xinshao formula on the cerebral ischemia reperfusion injury in rats. SD rats were randomly divided into five groups: sham operation group, model group, and low, middle and high-dose Xinshao formula groups (0.31, 0.62, 1.25 g·kg⁻¹). After administration with Xinshao formula for 7 days, the rats were used to establish the cerebral ischemia-reperfusion model. The neurological behavior was evaluated. TTC staining was implemented to determine the volume of cerebral infarction. The levels of ROS, SOD, GSH-PX, NO and iNOS in serum were examined, and the mRNA and protein levels of Bcl-2, Bax and caspase 3 in hippocampal CA1 were detected by qRT-PCR, immunohistochemical assay and Western blot. It is found that Xinshao formula could significantly reduce the symptoms of nervous function and the volume of cerebral infarction in MACO rats. Compared with model group, the rats in Xinshao formula group showed increases in the activities of SOD and GSH-PX (<0.01), and decreases in the activities of iNOS and the contents of NO, ROS and MDA (<0.01). In addition, Xinshao formula could down-regulate the mRNA and protein levels of Bax and caspase 3 (<0.01), and up-regulated those of Bcl-2 (<0.01) in MACO rats. In conclusion, Xinshao formula showed aprotective effect on cerebral ischemia reperfusion injuryin rats, which may be associated with the promotion of anti-oxidation and anti-apoptosis.

Structure and function of 3'- untranslated region in picornavirus / 病毒学报

Both sides of the picornavirus genome have 5'-untranslated region (5'UTR) and 3'- untranslated region (3'UTR). This study demontrated that both the 5'-and 3'-UTR can form complex structures, such as stem-loop, clover and pseudoknot structure, These structures play an important role in the regulaton of the replication and translation of the viruses. This article reviewed the progress of research on the structure and function of picornavirus' 3'-UTR over recent years.

Effect of micro - incision on corneal wavefront aberration and tear film in phacoemulsification / 国际眼科杂志(Guoji Yanke Zazhi)

AlM: To investigate the effect of endocapsular phacoemulsification cataract extraction and intraocular lens (lOL) implantation with a 1. 8mm or 3. 0mm clear corneal incision on total root mean square ( RMS ) value of the cornea, corneal astigmatism, spherical aberration, coma, trefoil and tear film. METHODS:ln a prospective study, 156 age- related patients ( 196 eyes ) were randomly distributed into two groups. 1. 8mm-group comprised 94 eyes that had a silicone lOL inserted through a 1. 8mm sutureless clear corneal incision, while, 3. 0mm- group comprised 102 eyes through a 3. 0mm clear corneal incision. Postoperatively, the changes in the total RMS value of the cornea, corneal astigmatism, spherical aberration, coma, trefoil and tear film at 1wk, 1 and 3mo were determined respectively. RESULTS:ln both groups, postoperatively at 1wk,there were statistically significant differences ( P 0. 05 ) between two groups at 3mo postoperative. CONCLUSlON:This study confirms that incision size has strong impact on the corneal higher-order aberrations, especially, 3. 0mm incision caused significant differences in the total RMS value of cornea, corneal astigmatism, spherical aberration, coma, trefoil and tear film compared with 1. 8mm micro-incision, therefore, micro-incision is very beneficial for clinical use in phacoemulsification.

Influence of recombinant thioredoxin on apoptosis of myocardium cell in viral myocarditis of mice / 中国地方病学杂志

ObjectiveTo investigate the influence of recombinant thioredoxin (TRX)on apoptosis of myocardium cell in viral myocarditis of mice.MethodsTwenty-four Balb/c mice,weighting 12 - 14 g,were randomly divided into 3 groups:the control group,the virus group and the protective group,8 mice in each group.The virus group and the protective group were injected with 0.1 ml 100TCID50 Coxackie virus B3 (CVB3)intraperitoneally,and the control group was injected equal volume of saline.Therewithal the protective group was injected with TRX(2 mg/kg) by tail vein,and the virus group was injected saline the same way.After 14 days all mice were killed and hearts were taken.Changes of myocardial histopathology was observed with optical microscope,cell apoptosis was checked by TUNEL technique,and the expression of apoptosis-related proteins (Bcl-2,caspase-3)in infiltrated cell of myocardium was determined by immunohistochemistry.Results(①)Lymphocyte infiltration and necrosis were observed in survivals of the virus group,sporadic coagulation necrosis and ballooning degeneration of cells were observed in the protective group,however no myocardial lesion was found in the control group.(②)TUNEL technique showed that the positive ratio of apoptosis in the virus group and the protective group[(90.23 ± 3.63)％,(20.02 ± 2.41)％] was significantly higher than that of the control group(0.00 ± 0.00,all P ＜ 0.05),the positive ratio of apoptosis in the protective group was significantly lower than that of the virus group (P ＜ 0.05 ).(③)Immunohistochemistry showed that the expression of protein Bcl-2(+,++,+++) in the virus group and the protective group was significantly higher than that of the control group (all P ＜ 0.05).The expression of protein Bcl-2 in the protective group was significantly higher than that of the virus group(P ＜ 0.05).The expression of caspase-3 (+,++) was significantly higher in the virus group and the protective group than the control group (all P ＜ 0.05).Compared with the virus group,the expression of caspase-3 in the protective group was significantly lower(P ＜ 0.05).ConclusionTRX could inhibit cardiomyocyte apoptosis in viral myocarditis mice and the inhibition is related to regulation of apoptosis-related protein expression.

Study on qi deficiency syndrome distribution and quality of life in patients with advanced non-small cell lung cancer / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To study the qi deficiency syndrome distribution and quality of life (QOL) of patients with advanced non-small cell lung cancer (NSCLC).</p><p><b>METHODS</b>A questionnaire survey was conducted in 120 patients with advanced NSCLC using the QOL scale "Functional Assessment of Cancer Therapy" (FACT-L) (Version 4.0). Meanwhile, syndrome typing was performed. On the basis of results of syndrome typing, patients of different syndrome types were grouped and compared, thus studying the distribution of advanced NSCLC patients of qi deficiency syndrome and qi deficiency syndrome correlated QOL features.</p><p><b>RESULTS</b>Qi deficiency, blood stasis, yin deficiency, phlegm and dampness dominated in syndrome types of the 120 patients with advanced NSCLC. Of syndrome types accounting for larger ratios in 112 patients, pure qi deficiency syndrome accounted for 30.36% (34 cases), qi deficiency and blood stasis syndrome for 18. 75% (21 cases), both qi and yin deficiency syndrome for 10. 71% (12 cases). There was no correlation between the appearance of qi deficiency syndrome and patients' age, sex, pathological typing (adenocarcinoma/squamous carcinoma), or the disease duration. NSCLC patients in phase IV were mostly complicated with qi deficiency syndrome (P<0.05). Scores of physical states, emotional states, functional states, and total scores in the FACT-L scale were lower in those complicated with qi deficiency syndrome (89 cases) than in those without complicated qi deficiency syndrome (31 cases), showing statistical difference (P<0.01, P<0.05). The scores of the lung cancer specific module (additional concerns) in the FACT-L scale showed statistical difference, sequenced as qi deficiency and blood stasis syndrome > pure qi deficiency syndrome > both qi and yin deficiency syndrome (P<0.05).</p><p><b>CONCLUSIONS</b>Qi deficiency syndrome is the main syndrome of advanced NSCLC. The QOL of advanced NSCLC patients complicated with qi deficiency syndrome was poorer than those without complicated qi deficiency syndrome. Besides, along with the aggravation of qi deficiency syndrome, the QOL decreased somewhat. It suggested that symptomatic treatment of qi deficiency syndrome could improve advanced NSCLC patients' QOL.</p>

Comparative study on the methods of Chinese medicine and Western medicine therapeutic evaluation for advanced non-small cell lung cancer / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To compare the differences and characteristics in Chinese medicine (CM) and Western medicine therapeutic evaluation methods in the application of advanced non-small cell lung cancer.</p><p><b>METHODS</b>A total of 200 cases of advanced non-small cell lung cancer from 3 subcenters were enrolled the study and assigned to two groups, 104 in the CM group treated with CM injection combined with treatment based on syndrome differentiation, 96 in the chemotherapy group treated with the international chemothearapy scheme, both the course of treatment was 6 weeks. Their short-term therapeutic effects were observed by the "clinic efficacy appraisal standard of therapy for advanced lung cancer with CM" simultaneously and by the follow-up Western medical solid tumor's effect evaluation criterion, including clinical symptoms, tumor body, Karnorfsky score, body weight and immune function evaluation.</p><p><b>RESULTS</b>According to WHO solid tumor's effect evaluation criterion, the efficacy of the chemotherapy group was much better than that of the CM group (P < 0.01). While, according to the "clinic efficacy appraisal standard of therapy for advanced lung cancer with CM", the efficacy of the CM group was better than that of the chemotherapy group without statistical difference (P = 0.05), however, there was a very strong trend of appearing difference. There was difference inult o the results of the two evaluation methods.</p><p><b>CONCLUSION</b>Compared with WHO solid tumor's effect evaluation criterion, "the clinic efficacy appraisal standard of therapy for advanced lung cancer with CM" can reflect more features and advantages of CM for cancer treatment, having value for further study.</p>

Roles of UGT 1A1 gene mutation in the development of neonatal hyperbilirubinemia in Guangxi / 中华儿科杂志

<p><b>OBJECTIVE</b>Neonatal unconjugated hyperbilirubinemia is one of the most common conditions encountered by the practicing pediatricians. Although it is usually self-limited and benign, the condition is of importance because of the rare instances in which severe hyperbilirubinemia can lead to bilirubin encephalopathy or kernicterus. The uridine diphosphate-glucuronosyl transferase 1A1 (UGT 1A1) gene controls bilirubin conjugation by determining the structure of the enzyme glucuronosyltransferase, which is synthesized in the hepatocyte. In the recent years much has been learned about the relationship between UGT 1A1 gene mutation and neonatal hyperbilirubinemia. This study aimed to investigate the roles of UGT 1A1 gene mutation in the development of neonatal hyperbilirubinemia in Guangxi.</p><p><b>METHODS</b>A total of 73 cases with hyperbilirubinemia and 31 healthy neonates were enrolled. UGT 1A1 G71R genotypes were identified by the (amplification refractory mutation system, ARMS) and direct sequencing method in all the neonates. To analyze the incidence of bilirubin encephalopathy, the peak (total serum bilirubin, TSB) concentration after 72 hours of age, and the possibility of TSB > 20 mg/dl of each group.</p><p><b>RESULTS</b>(1) The frequencies of allele G71R were 0.1915 in this study, 0.2329 in hyperbilirubinemia group vs. 0.097 in healthy groups. The allele gene frequency of G71R in neonatal hyperbilirubinemia was higher than that in the normal group (P < 0.05). (2) Homozygous neonates had higher possibility to develop bilirubin encephalopathy and higher TSB concentration 72 hours after birth (28.57%, 23.12 ± 4.58) than the normal group (0%, 17.68 ± 2.69). The difference between the former two was significant (P < 0.001). (3) The TSB of the 5 neonates was > 20 mg/dl in G71R homozygous type, the odds ratio and 95%CI were 7.955 (1.349, 46.899).</p><p><b>CONCLUSION</b>(1) G71R mutation gene was associated with neonatal jaundice in Guangxi region. (2) The possibility of TSB > 20 mg/dl in G71R homozygous was higher than those of the wild-type. (3) The incidence of bilirubin encephalopathy and TSB concentration after 72 hours of age for neonates who were homozygous to G71R gene were higher than the wild-type.</p>

Effect of recombinant human thioredoxin on Coxsackie virus 3m-induced cell injury / 中国地方病学杂志

Objective To observe the protective function of recombinant human thioredoxin(TRX) on HeLa cell injury induced by Coxsackie virus 3m(CVB3m) and to study the inhibiting effect of TRX on viral replication. Methods We infected HeLa cells with 10TCID50 CVB3m and then protected these cells with TRX (2,5,10 mg/L). The protective group of TRX, viral group, control group of TRX, and normal control group were included. Six parallel wells were set up in each group. The cell growth was observed by methyl thiazolyl tetrazolium(MTT) and contrast phase microscope. Results The results of contrast phase microscope revealed that HeLa cells were arranged tightly and polygon in normal control group; untightly, became circle and abscission in viral group; HeLa cells morphous improved by increasing TRX concentration in TRX protective group(2,5,10mg/L). MTT results of the inhibitory ratio on cell growth of TRX(2,5,10 mg/L) control group(1.2%,2.9%,6.3%) were compared with normal control group(0), there was no significant difference(all P > 0.05); and while the inhibitory ratio on cell growth of TRX(2,5,10 mg/L) protective group(32.0%,28.0%,27.0%) was compared with virus infective group(51.7%), there was a significant difference (all P < 0.05). The inhibition study of viral replication showed that compared the inhibitory ratio on cell growth of TRX(2,5,10 mg/L) protective group(26.0%,27.0%, 10.9%) with virus infective group(60.0%), there was a significant difference(all P < 0.05). In the protective groups, there was a significant difference (all P < 0.05) between low dose groups(2,5 mg/L) and high dose groups( 10 mg/L). Conclusions The recombinant TRX(2,5,10 mg/L) may alleviate HeLa cell's injury induced by virus and the construct has no significant toxicity. TRX(2,5,10 mg/L) is effective in inhibiting virus CVB3m replication.

Relationship between glucose-6-phosphate dehydrogenase gene mutations and neonatal jaundice in Naning, Guangxi / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the correlation between glucose-6-phosphate dehydrogenase (G-6-PD) activities and three common mutations of G-6-PD gene G1388A, G1376T and A95G and investigate the effects of G-6-PD gene mutations on neonatal jaundice in Nanning, Guangxi.</p><p><b>METHODS</b>One hundred and twenty-four neonates from Nanning, Guangxi, with hyperbilirubinemia were enrolled. The ARMS-PCR and PCR/REA methods were used to determine G-6-PD gene mutations. G-6-PD activities were measured using the NBT method. The incidence of acute bilirubin encephalopathy and the peak bilirubin concentration 72 hrs after birth were compared between the neonates with different genotypes and between the G-6-PD mutation and normal groups. The risk of blood serum bilirubin >340 mumol/L was evaluated by logistic regression analysis.</p><p><b>RESULTS</b>Of the 124 cases, gene mutations were found in 37 cases, including G1388A (n=20), G1376T (n=14), A95G (n=4) and G1388A+A95G (n=1). Five cases (25%) showed normal G-6-PD activities in the G1388A gene mutation group and 4 (29%) had normal G-6-PD activities in the G1376T G1388A gene mutation group. All of 4 cases of A95G G1388A gene mutation showed a deficiency of G-6-PD activities. There were no significant differences in the incidence of acute bilirubin encephalopathy and the peak bilirubin concentration 72 hrs after birth between the G1388A and G1376T G1388A gene mutation groups. The incidence of acute bilirubin encephalopathy, the peak bilirubin concentration 72 hrs after birth and the risk of serum bilirubin >340 micromol/L in the G-6-PD mutation group were not different from the normal group.</p><p><b>CONCLUSIONS</b>G1388A, G1376T and A95G are common G-6-PD gene mutations in Nanning, Guangxi. The false negative results may be received when the NBT method is used for diagnosis of G-6-PD deficiency. There are similar effects on the incidence of acute bilirubin encephalopathy and the peak bilirubin concentration 72 hrs after birth between different gene mutation groups. G-6-PD gene mutations alone may not contribute to the development of acute bilirubin encephalopathy and the changes of peak bilirubin concentration 72 hrs after birth and the risk of serum bilirubin >340 micromol/L.</p>

Human thioredoxin exerts cardioprotective effect and attenuates reperfusion injury in rats partially via inhibiting apoptosis / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Thioredoxin is one of the most important redox regulating proteins. Although thioredoxin has been shown to protect cells against different kinds of oxidative stress, the role of thioredoxin in myocardial ischemia and reperfusion injury has not been fully understood. This study was conducted to explore the protective role of human thioredoxin on myocardial ischemia and reperfusion injury and its potential mechanisms.</p><p><b>METHODS</b>Purified human thioredoxin was injected into adult Wistar rats, which were subjected to 30 minutes of myocardial ischemia followed by 2 or 24 hours of reperfusion. We detected 1) the infarct size; 2) the level of malondisldehyde (MDA) in serum; 3) the expression of caspase-9, and cytochrome c in/out of mitochondria by Western blotting; 4) apoptosis by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) assay and caspase-3 and its protein by reverse transcriptase polymerase chain reaction (RT-PCR) and Western blotting; 5) the expression of bcl-2 and bax in cardium by immunohistochemical (IHC) assay.</p><p><b>RESULTS</b>Human thioredoxin reduced myocardial ischemia/reperfusion injury as evidenced by significant decrease of myocardial infarct size (P < 0.01), notable reduction of myocyte apoptosis (P < 0.01), lower systemic oxidative stress level (P < 0.01) after reperfusion for 2 hours, and few inflammatory cell infiltration after reperfusion for 24 hours in rats. Furthermore, treatment with human thioredoxin significantly reduced the release of mitochondrial cytochrome C (P < 0.05), and inhibited the activity of caspase-9 (P < 0.05) and caspase-3 (P < 0.01 in mRNA and P < 0.05 at protein level). Meanwhile, human thioredoxin markedly increased bcl-2 expression (P < 0.05).</p><p><b>CONCLUSIONS</b>These results strongly suggest that human thioredoxin has cardioprotective effects on myocardial ischemia/reperfusion and its anti-apoptotic role may be mediated by modulating bcl-2 and the mitochondria-dependent apoptotic signaling pathway.</p>

Protective effects of recombinant human thioredoxin on myocardium in mice with viral myocarditis / 中国地方病学杂志

Objective To evaluate protective effects of recombinant human thioredoxin(TRX) in myocardial injury of mice with viral myocarditis. Methods We established viral myocarditis models by intraperitoneal injection with 0.1 ml 100TCID50 Coxsackie virus 3m(CVB3m), along with tail vein injection of recombinant human TRX (2 mg/kg) for protection. The control group was given equivalent volume of normal saline. The mice were killed 7 days following the injections. Serum lactate dehydrogenase (LDH) activity was determined and myocardial injury was examined with light microscopy. Results The somm LDH activity in Coxsackie virns-infected mice [(3130.50±390.57)U/L] was higher than that of animals in the control group[ (1617.86±155.42)U/L] and that of TRX protection group[ (1959.43±540.75)U/L], the difference being statistically significant (P<0.05); there was no significant difference between TRX protection group and the control group(P 0.05). Light microscopy showed that five of the eight Coxsackie rims-infected mice had myocardial lesions, including focal myocardial necrosis and inflammatory infiltration. There was no myocardial injury in the TRX protection group. Conclusions Recombinant human TRX can lessen myocardial injuries induced by infection with CVB3m, and so can protect myocardium.