OBJECTIVETo investigate the protect effects of sodium ferulate (SF) on the daunormbicin(DNR-induced cardiotoxicity in juvenile rats.

METHODSForty male juvenile SD rats were randomly divided into control group (Control), daunorubicin group (DNR), sodium ferudate treatment group (DNR + SF), sodium ferudate group (SF) (n = 10) . Juvenile rats were intraperitoneally treated with DNR (2.5 mg/kg every week for a cumulative dose of 10 mg/kg) preparation immature myocardial injury model in presence with SF (60 mg/kg) oral treat- ment for 25 days. The left ventricular pressure and its response to isoproterenol were measured using left ventricular catheter. Rat myocardium myocardial pathology specimens and ultrastructure changes were also observed. The expression of cardiac Troponin I (cTNI) was detected by Western blot and RT-PCR. Results: SF treatment could inhibit the decreasing of heart rates induced by DNR damage (P < 0.05); it could increase the left ventrivular end diastolic pressure(LVEDP), heart rate, the maximal left ventrivular systolic speed(LVP + dp/dtmax) and the maximal left ventrivular diastolic speed (LVP-dp/dtmax) responding to isoproterenol stimulation(P < 0.01); SF also could improve the myocardial ultrastructure injuries and inhibit the decreasing of cTNI expression caused by DNR damages (P < 0.05).

CONCLUSIONSF treatment could alleviate the decreasing of cardiac reservation induced by DNR damages in juvenile rats, which might be related to its reversing the effects on the cardiac systolic and diastolic function injuries and its inhibiting effects on the decreasing of cTNI expression caused by DNR. The mechanism of SF preventing daunorubicin-induced cardiotoxicity in juvenile rats is relevant to inhabited cardiac Troponin I expression.

Animals ; Blood Pressure ; Cardiotoxicity ; drug therapy ; Coumaric Acids ; pharmacology ; Daunorubicin ; toxicity ; Heart ; physiopathology ; Heart Rate ; Isoproterenol ; Male ; Myocardium ; pathology ; Protective Agents ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Troponin I ; metabolism

Animals ; Animals, Newborn ; Chronic Disease ; Daunorubicin ; adverse effects ; Disease Models, Animal ; Heart Failure ; chemically induced ; Rats ; Rats, Sprague-Dawley

BACKGROUND:To dynamicaly monitor the varying levels of inflammatory factors in the gingival crevicular fluid is helpful to assess the early effect of orthodontic tooth movement. Myeloperoxidase, soluble intercelular adhesion molecule-1, pentraxin 3 are proven to be closely related to inflammation, but it is unclear about the levels of these three kinds of inflammatory factors as wel as association of these three kinds of inflammatory factors with orthodontic tooth. OBJECTIVE:To detect the expression levels of myeloperoxidase, soluble intercelular adhesion molecule-1 and pentraxin-3 in the gingival crevicular fluid during maxilary canine distal movement and to assess their correlation with periodontal disease, canine movement distance and orthodontic force. METHODS:Twenty-one orthodontic patients were enroled and assigned into 150 g (n=12) or 100 g (n=9) groups according to orthodontic force. The gingival crevicular fluid samples of orthodontic patients were colected before and at 4, 12, 24 hours, 7, 14 days after maxilary canine distal movement. Levels of myeloperoxidase, soluble intercelular adhesion molecule-1 and pentraxin-3 in the gingival crevicular fluid were measured and analyzed using ELISA assay. RESULTS AND CONCLUSION: During the distal movement of maxilary canine, under orthodontic force, the level of myeloperoxidase was peaked at 4 hours and then decreased, while the expression level of soluble intercelular adhesion molecule-1 was peaked at 12 hours, and then decreased. Both myeloperoxidase and soluble intercelular adhesion molecule-1 levels returned to normal at 7 days under orthodontic force. The expression level of pentraxin-3 was increased significantly under orthodontic force, peaked at 24 hours, and then decreased gradualy to the normal level at 7 days. In addition, the expression levels of myeloperoxidase, soluble intercelular adhesion molecule-1 and pentraxin-3 in the gingival crevicular fluid were significantly higher under 150 g force than under 100 g force. These findings indicate that detecting varying levels of myeloperoxidase, soluble intercelular adhesion molecule-1 and pentraxin-3 in the gingival crevicular fluid is useful to assess the efficiency of orthodontic treatment and prevent adverse reactions.

OBJECTIVETo compare the difference in the clinical efficacy on cervical spondylosis of vertebral artery type (CSA) treated with thermosensitive moxibustion at different dosages.

METHODSSixty cases of CSA were randomized into a saturated moxa dosage group and a regular moxa dosage group, 30 cases in each one. The thermosensitive moxibustion was adopted in the two groups. The mild suspended moxibustion was applied at two acupoints with the strongest thermosensitization. In the saturated moxa dosage group, the moxibustion time was determined by the disappearance of thermosensitization. In the regular moxa dosage group, 15 min was required on each acupoint. The treatment was given twice a day for first 4 days in the two groups. Since the 5th day, the treatment was given once a day, continuously for 10 times, and totally 14 days were required. The score of symptoms and function and clinical efficacy were compared between the two groups before and after treatment as well as 6-month follow-up after treatment.

RESULTSThe curative and effective rate was 56.7% (17/30) after treatment and 60.0% (18/30) in 6-month follow-up after treatment in the saturated moxa dosage group, which were superior to 26.7% (8/30) and 30.0% (9/30) in the regular moxa dosage group respectively (P < 0.01, P < 0.05). The scores of clinical symptoms and function after treatment and in follow-up were improved apparently as compared with those before treatment in both groups (all P < 0.01). The scores of clinical symptoms and function after treatment and in follow-up in the saturated moxa dosage group were increased much more apparently than those in the regular moxa dosage group (after treatment: 22.32 +/- 4.64 vs 17.43 +/- 3.21; in follow-up: 23.01 +/- 4.76 vs 18.32 +/- 2.13, both P < 0.01).

CONCLUSIONThe thermosensitization moxibustion of saturated dosage achieves the superior short-term and long-term efficacies in the treatment of CSA as compared with the regular moxibustion dosage.

Acupuncture Points ; Adult ; Female ; Humans ; Male ; Middle Aged ; Moxibustion ; instrumentation ; Spondylosis ; physiopathology ; therapy ; Vertebral Artery ; physiopathology

OBJECTIVETo summarize our experiences with the treatment of non-small cell lung cancer (NSCLC) with cetuximab and compare the therapeutic effects of cetuximab applied in the first line and non-first line settings.

METHODSFrom October 1, 2006 to December 31, 2009, 16 NSCLC patients were treated with cetuximab combined with standard chemotherapy in Sun Yat-sen University Cancer Center. The short-term efficacy of the therapeutic protocols were analyzed.

RESULTSA total of 115 cycles of cetuximab treatment were administered in these patients with a median of 6 cycles (7.5 in the first line setting and 2 in non-first line setting). In the 10 patients with cetuximab treatment in the first line setting, the ORR was 40.0% (4/10), DCR was 80.0% (8/10), median TTP was 6.5 months (2-19), and median OS was 8.5 months (2-48); in the non-first line setting, these indices were 33.3% (2/6), 33.3% (2/6), 3.5 months (3-4) and 18 months (4-28), respectively. Both ORR and DCR were similar between the first and non-first line settings (P=0.790, P=0.062). Ten of the patients (62.5%) developed acne-like rash within 3 weeks, who had an ORR of 60% (6/10) and DCR of 90% (9/10); the ORR and DCR in patients without acne-like rash were both 10.4% (1/6), showing no significant difference in ORR (P=0.080) but a significant difference in DCR between the two groups (P=0.003). No treatment-associated death or cetuximab-associated discontinuation occurred. Altogether 11 patients (68.8%) developed acne-like rash, which occurred within 3 weeks in 10 cases. Seven patients showed side effects associated with the chemotherapy.

CONCLUSIONCetuximab combined with standard chemotherapy is a good option for Chinese patients with NSCLC and the current data support the application of cetuximab in the first line setting.

Adult ; Aged ; Antibodies, Monoclonal, Humanized ; administration & dosage ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Carcinoma, Non-Small-Cell Lung ; drug therapy ; Cetuximab ; Female ; Humans ; Lung Neoplasms ; drug therapy ; Male ; Middle Aged ; Treatment Outcome

The aim of the present study is to investigate the effects of Panax notoginseng saponins (PNS) on pneumocyte apoptosis and apoptosis-related protein, as well as c-Jun N-terminal kinase (JNK) in lung ischemia/reperfusion (I/R) injury. Thirty Wistar rats were randomly divided into control group, I/R group and PNS group. The unilateral lung I/R model was replicated by obstruction of left lung hilus for 30 min and reperfusion for 120 min in vivo. The rats in PNS group were given intraperitoneal injection of PNS at 60 min before ischemia and 10 min before reperfusion. Some lung tissues sampled at the end of the experiment were assayed for wet/dry weight ratio (W/T). The expressions of phosphorylated JNK (p-JNK) and JNK protein were detected by Western blot. The expressions of Bcl-2, Bax and Caspase-3 protein were detected by immunocytochemistry techniques. The pneumocyte apoptotic index (AI) was detected by terminal deoxynuleotidy1 transferase mediated dUTP nick end labeling (TUNEL). The morphological and ultrastructure changes were observed under light microscope and electron microscope, and the injured alveolus rate (IAR) was counted as well. The results showed that compared to control group, I/R group showed increased expressions of p-JNK, Bcl-2, Bax and Caspase-3 protein (all P < 0.01), decreased ratio of Bcl-2/Bax (P < 0.05), and increased values of AI, W/T and IAR (all P < 0.01). Moreover, light microscope and electron microscope showed serious morphological and ultrastructure injury in I/R group. Compared to I/R group, PNS group showed markedly decreased expressions of p-JNK, Bax and Caspase-3 protein (all P < 0.01), increased expression of Bcl-2 protein and ratio of Bcl-2/Bax (both P < 0.01), and lower values of AI, W/T and IAR (all P < 0.01). Meanwhile, light morphological and ultrastructure injury was found to be alleviated in PNS group. These results suggest that PNS can protect lung tissue from I/R injury, and the mechanism may correlate with suppressing JNK signal pathway, up-regulating the ratio of Bcl-2/Bax which results in inhibition of Caspase-3 dependent apoptosis.
Alveolar Epithelial Cells ; drug effects ; Animals ; Apoptosis ; drug effects ; Female ; Ischemia ; physiopathology ; JNK Mitogen-Activated Protein Kinases ; metabolism ; Lung ; blood supply ; metabolism ; pathology ; Male ; Panax notoginseng ; chemistry ; Rats ; Rats, Wistar ; Reperfusion Injury ; prevention & control ; Saponins ; isolation & purification ; pharmacology ; Signal Transduction ; drug effects

OBJECTIVETo study a simple and reliable method to produce the rat model of alcoholic cardiomyopathy, evaluating the model with isoprenaline provocation test (IPT) and morphological indicators.

METHODSAdult male rats were intragastrically infused of wine (52% v/v) at 20 g/(kg x d) for 15 days with the general condition, the change of eating amount and weight being observed. The levels of mean left ventricle systolic pressure (mLVSP), mean left ventricle diastolic pressure (mLVDP), mean left ventricle pressure (mLVP), heart ratio (HR), maximal rise velocity of left ventricular pressure (+ dp/dtmax), maximal fall velocity of left ventricular pressure (- dp/dtmax) and the reaction of isoprenaline were examined by left ventricular cannulation, and the morphological change was observed with optical microscope and transmission electron microscopy.

RESULTSBoth diastolic and systolic function of the model rats was lower than that of the control group as well as the cardiac energy reserve induced by IPT. Pathological observation demonstrated myocardial hypertrophy, myocardiocyte necrosis and infiltration of inflammatory cells. The transmission electron microscopy showed that mitochondria became enlarged or crimpled with fused or disappeared cristae and myofibrils dissolved and fractured.

CONCLUSIONThe adult male SD model rats exhibit diabetic cardiomyopathy by intragastric infusion of wine (52% v/v) at 20 g/(kg x d) for 15 days. IPT can induce the cardiac energy reserve and evaluate that accurately, displaying the hidden heart dysfunction.

Animals ; Cardiomyopathy, Alcoholic ; physiopathology ; Disease Models, Animal ; Isoproterenol ; Male ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate the protective effects and mechanism of SP600125-specificity inhibitor of c-Jun N-terminal kinase (JNK)on lung ischemia /reperfusion injury in rats.

METHODSThe unilateral lung ischemia/reperfusion model was replicated in vivo. Rats were randomly divided into three groups (n = 10): control group, ischemia/reperfusion group ( I/R group) and ischemia/reperfusion + SP600125 group (SP600125 group). The lung tissues sampled at the end of each experiment were assayed for wet/dry weight ratio (W/D),the injured alveoli rate (IAR), the expression of phosphorylation JNK (p-JNK) and JNK protein were detected by Western blot, the expression of Bcl-2, Bax, Caspase3 protein were detected by immunocytochemistry techniques, the pneumocyte apoptosis index (AI) was detected by terminal deoxynucleotidyl transferase mediated dUTP nick end abeling(TUNEL), the ultrastructure changes were observed under electron microscope.

RESULTSCompared to I/R group, the expression of p-JNK, Bcl-2, Bax and caspase-3 protein were markedly decreased (all P < 0.01), the expression of Bcl-2 protein and the ratio of Bcl-2/Bax were markedly increased in SP600125 group(all P < 0.01). The value of AI, W/D, IAR showed significantly lower than those in I/R group (all P <0.01). Meanwhile, light morphological and ultrastructure injury were found in SP600125 group.

CONCLUSIONSP600125 can suppress JNK signal pathway, up-regulate the ratio of Bcl-2/Bax to inhibit Caspase-3 dependent apoptosis, so that it protects lung tissue from ischemia/reperfusion injury.

Animals ; Anthracenes ; pharmacology ; Apoptosis ; drug effects ; Caspase 3 ; metabolism ; Lung ; blood supply ; metabolism ; pathology ; MAP Kinase Signaling System ; Phosphorylation ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Rats ; Rats, Wistar ; Reperfusion Injury ; metabolism ; pathology ; bcl-2-Associated X Protein ; metabolism

OBJECTIVETo explore the appropriate temperature of the kalium-verapamil-propranolol (KVP) cardioplegia by observation of the effect on the function of the immature rat heart.

METHODSIsolated hearts from immature rats were perfused by Langendorff method, and assigned to 1 of the following 5 groups (n = 6-8): control, continuously perfused for 170 min at 36 degrees C, normal temperature, normal perfused for 20 min, changed to perfuse with KVP for 3 min then no perfusion 87 min (ischemia 90 min), followed by 60 min reperfusion. 3 groups of low temperature, perfused for 15 min, cool down to 32 degrees C, 28 degrees C and 24 degrees C especially in 5 min, and at 20th min. heart rate (b/min), tension (g), contraction force (g), peak systolic velocity (dT/dt(max)), peak diastole velocity (dT/dt(max)), coronary flow (Drop/min) were monitored during the whole perfusion.

RESULTSCompared to control group, the heart tension increased after 50 min KVP ischemia. The protection of KVP in normal temperature (36 degrees C) was better than lower temperature (32 degrees C, 28 degrees C, 24 degrees C) such as reducing bad contraction, keeping normal myocardium tension,recovering heart rate, recovering the fuction of contraction force and protecting the coronary flow.

CONCLUSIONThe KVP cardioplegia in normal temperature has the better effect than that in hypothermia to protect the immature heart.

Animals ; Cardioplegic Solutions ; pharmacology ; Heart ; physiopathology ; Heart Arrest, Induced ; In Vitro Techniques ; Male ; Myocardial Reperfusion Injury ; prevention & control ; Rats ; Rats, Sprague-Dawley ; Temperature ; Ventricular Dysfunction ; prevention & control

Objective To investigate the clinical effect of angioplasty for symptomatic intracranial atherosclerotic stenosis. Methods Eighty-two patients with symptomatic intracranial atherosclerotic stenosis whom underwent angioplasty after the failure of standard medical therapy were enrolled from Nan-jing Stroke Registry Program from September 2010 to June 2013.Nine of them underwent routine balloon angioplasty alone and 73 underwent intracranial stenting.The median time from onset to surgery was 24.5 days.The occurrence of endpoint events (any stroke ≤30 d after procedure,death and ischemic stroke >30 d in guilty vessels or original stenosis had restenosis and needed to be treated again)was assessed. The incidence of restenosis was followed up with imaging (CTA or DSA). Results (1)In the 82 patients, the success rate of operation was 92.7%(n=72 ),and 78 (95.1%)received follow-up,4 were lost to follow-up.The median follow-up time was 22.5 months (range 9 to 29 months ).Ten patients had an endpoint event,7 of them were ischemic stroke,1 was cerebral hemorrhage,and two were severe asymptomatic restenosis who underwent stenting again.The endpoint events of 3 patients occurred at day 30 after procedure (at ≤24 h after procedure).Kaplan-Meier curves showed that the incidences of cumulative endpoint events at 1,6,12,and 24 months were 3.7%,8.6%,11%,and 13%,respectively.(2)60 patients (73.2%)received imaging examination (11 CTA and 49 DSA ).Restenosis occurred in 17 patients (28.3%),among them the incidence of symptomatic restenosis was 5%(n =3 ),and asymptomatic restenosis was 23.3%(n=14). Conclusion After a comprehensive assessment and a rigorous screening, the safety is high and the mid- and long-term efficacy are satisfactory in patients with symptomatic intracranial arterial stenosis who are treated with angioplasty when their medical treatment is invalid.