Objective To establish an animal model of severe bone marrow type acute radiation sickness in the BALB/c mice and to provide a good foundation for further investigation of severe bone marrow type acute radiation sickness.Methods BALB/c mice were given 6.0 Gy 60Co γ-rays total body irradiation.The mice were observed twice a day.The changes in body weight,peripheral blood cell counts were recorded once every three days.Histopathological sections of femur were prepared to observe the histomorphological changes.Bone marrow cells were collected to perform colony cultivation on day 1 before irradiation,and 14 d,28 d after irradiation.Results The mice were less active three days after irradiation,but there were no vomiting and loose stools.The white blood cell counts were dropped to the nadirs (3.0 ％) 11 days after irradiation and recovered to 53.7 ％ on day 28 after irradiation.The platelet counts were dropped to the nadirs (8.1％) 14 days after irradiation and recovered to 60.4 ％ on day 28 after irradiation.Histopathological section showed that the bone marrow cavity was almost empty on day 14 after irradiation.Semi-solid bone marrow cell culture results also demonstrated that CFU-GM and CFU-Mix were obviously decreased.They were not yet fully recovered on day 28 after irradiation.All mice were still alive two months after irradiation.Conclusion A murine model of severe bone marrow type acute radiation sickness has been successfully established by exposure to 6.0 Gy 60Co γ-rays.

ObjectiveTo investigate the influence of Tanshinone Ⅱ A on the expression of HMGB1 in rats with cerebral ischemia-reperfusion (I/R) injury and its neural function protection.MethodsThe 32 male SD rats were randomly (random number) divided into 4 groups (8 rats per group):Sham group,I/R group,group with low dose of Tanshinone Ⅱ A ( TaLD group) and group with high dose of Tanshinone Ⅱ A (TaHD group).The cerebral I/R models were established by the method of right middle cerebral artery occlusion (MCAO).Cerebral infarct volume was detected by TTC staining.Apoptotic cell and apoptotic index were calculated by Tunnel assay.The HMGB1 levels in brain and serum was detected by Western blot and ELISA.Calmodulin (CaM) activity and malondialdehyde (malondiadehyde,MDA) content in the brain were also detected.ResultsCompared with the Sham group,the volume of cerebral infarction,the number of apoptotic cells,CaM activity,MDA content,HMGB1 levels in the brain tissue and serum in group I/R,TaLD group and TaHD group increased significantly (P ＜ 0.01 ).Compared with the group I/R,the volume of cerebral infarction,the number of apoptotic cells,CaM activity,MDA content and the HMGB1 levels in brain tissue and serum in TaLD groupand TaHDgroup decreased significantly (P ＜ 0.01 ).The difference of the above index between TaLD groupand TaHDgroup was significant ( P ＜ 0.01 ).ConclusionsTan Ⅱ A could reduce the cerebral ischemic reperfusion injury in rats which was likely related with decreasing the inflammatory response in the late stage via HMGB1.

Objective To investigate the protective effect of electroacupuncture pretreatment on myocardial ischemia/reperfusion (I/R) injury and its influence on high mobility group box 1 (HMGB1) expression in rats. Methods Sixty Wistar rats were randomly divided into sham operation group, myocardial I/R model group and electroacupuncture pretreatment group by random number table (each n = 20). Myocardial I/R injury model was reproduced by ligating the left ventricular branch coronary artery at about 0.5 cm below the atrial appendage lower margin for 10 minutes to occlude the blood flow, then the ligature was relaxed for 1 hour reperfusion; in electroacupuncture pretreatment group, 7 days before I/R, the electroacupuncture at Neiguan acupoint was applied once daily for 20 minutes till the 7th day when I/R was established. Under light microscope, the pathological changes of myocardial specimen stained by hematoxylin-eosine (HE) method were observed. The myocardial histopathological integral was detected by semi quantitative integral method, and the changes of histological scores in three groups were investigated. The levels of plasma HMGB1, tumor necrosis factor-α (TNF-α), cardiac troponin T (cTnT) were detected by enzyme-labeled immunosorbent assay (ELISA). The expressions of HMGB1, monocyte chemotactic protein-1 (MCP-1), TNF-αmRNA and protein in myocardium were detected by reverse transcription-polymerase chain reaction (PT-PCR) and Western Blot. Results Under light microscope, the myocardial tissue in myocardial I/R model group showed partial fracture of myocardial fibers, large patches of myocardial cell necrosis, hazy boundary, cellular condensation, rupture and dissolution or even disappearance, interstitial edema with a lot of inflammatory cell infiltration; the above myocardial tissue injury in electroacupuncture pretreatment group was significantly milder than that in myocardial I/R model group. Compared with sham operation group, in myocardial I/R model group the HMGB1, TNF-α, cTnT contents and histological score were significantly increased [HMGB1 (μg/L):9.64±1.16 vs. 2.15±0.31, TNF-α(μg/L):91±22 vs. 19±5, cTnT (μg/L):1.50±0.35 vs. 0.07±0.03, histological score:2.5±0.3 vs. 0.0±0.0, all P<0.01], HMGB1, MCP-1, TNF-α mRNA and protein expressions were increased obviously (HMGB1 mRNA: 1.42±0.16 vs. 0.02±0.00, MCP-1 mRNA:0.46±0.06 vs. 0.01±0.00, TNF-αmRNA:0.75±0.04 vs. 0.03±0.00;HMGB1 protein:1.08±0.01 vs. 0.20±0.01, MCP-1 protein:0.92±0.03 vs. 0.40±0.01, TNF-αprotein:1.10±0.02 vs. 0.35±0.01, P<0.05 or P<0.01);compared with myocardial I/R model group, in electroacupuncture pretreatment group, HMGB1 (6.58±0.73), TNF-α (63±19), cTnT (1.15±0.31) levels were significantly decreased (all P < 0.01), HMGB1, MCP-1, TNF-αmRNA and protein expressions were markedly reduced (mRNA expression was 0.74±0.12, 0.18±0.02, 0.10±0.03, and protein expression was 0.40±0.01, 0.36±0.02, 0.50±0.02, respectively all P<0.05), and histological score (1.2±1.0) was remarkably lowered (P < 0.01). Conclusion Electroacupuncture pretreatment may reduce the myocardial I/R injury in rats, and the mechanism may be related to the amelioration of inflammatory response mediated by HMGB1 at late stage.

ObjectiveTo investigate the protective effect of tanshinoneⅡA on the expression of S100A1 protein after acute myocardial ischemia injury in rats.Methods Sixty Wistar rats were randomly divided into sham operation group, acute myocardial ischemia model group and tanshinoneⅡA pretreatment group by random number table. The acute myocardial ischemia model was established by thoracotomy and penetration of a thread and occlusion around the root part of the left anterior descending coronary artery, while the sham operation group was established only by thoracotomy and penetration of a thread around the root part of that artery but without occlusion; 3 days before the operation, in the tanshinoneⅡA pretreatment group, intraperitoneal injection of tanshinoneⅡA solution(at a dose of 1.5 mg/kg) was applied, while in the sham and acute myocardial ischemia groups, intraperitoneal injection of an equal volume of saline was given. Myocardial cell apoptosis was detected by the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling(TUNEL), the levels of serum superoxide dismutase (SOD), malondialdehyde(MDA), creatine kinase(CK), lactate dehydrogenase(LDH) and S100A1 protein were examined and the level of expression of S100A1 protein in myocardial tissue was assayed by immunohistochemical staining and Western Blot.Results Compared with the sham operation group, the myocardial cell apoptosis rate, the contents of MDA, CK, LDH, S100A1 and the level of S100A1 expression in myocardial ischemia group and tanshinoneⅡA pretreated group were significantly increased, while SOD activity was decreased obviously; compared with the myocardial ischemia model group, the myocardial cell apoptosis rate, the contents of MDA, CK, LDH, S100A1 and the level of S100A1 protein expression were significantly reduced〔apoptosis rate:(32.1±4.2)% vs.(72.4±5.4)%, MDA(μmol/L): 9.1±2.2 vs. 17.3±5.2, CK(U/L): 83.3±12.2 vs. 107.5±12.4, LDH (μmol·s-1·L-1): 84.0±16.4 vs. 114.4±16.0, S100A1(μg/L): 37.6±6.0 vs. 78.4±8.6,P<0.05 orP<0.01〕, while the activity of SOD was increased markedly in tanshinoneⅡA pretreated group(kU/L:72.8±10.2 vs. 49.6±8.8,P<0.01). TUNEL staining showed that in the myocardial ischemia model group and tanshinoneⅡA pretreated group, the myocardial cells represented positive staining(brown-yellow in color), irregular in shape with nuclear pyknosis, cell detachment from the surrounding tissue and other characteristics. And in sham operation group,the staining of majority of cells was negative. The results of immunohistochemistry showed that S100A1 protein staining was relatively deep in the myocardial ischemia model group and tanshinoneⅡA pretreated group, and in the latter group, the color of S100A1 protein positive staining was not as deep as that in the former group. Western Blot showed that the S100A1 protein expression in myocardial ischemia model group was 2.8 folds of that of the sham operation group, while the S100A1 protein expression in tanshinoneⅡA pretreated group was significantly decreased compared with that of myocardial ischemia model group(bothP<0.05),which was 1.5 folds of that of the sham operation group.ConclusionTanshinoneⅡA may play a role in inhibiting the expression of S100A1 protein to protect against acute myocardial ischemia injury, suggesting that this agent have a potential effect for treatment of myocardial ischemia.

Objective: To summarize and discuss the clinical effect of Shiquan Dabu Decoction combined with nitroglycerin in the treatment of heart failure after acute myocardial infarction. Methods: From January 2016 to June 2017, 110 patients with heart failure after acute myocardial infarction admitted to the Department of Cardiology of Lishui Hospital of Traditional Chinese Medicine were selected as study objects.The patients were randomly divided into observation group and control group according to the digital table, with 55 cases in each group.The control group was treated with routine nitroglycerin therapy, while the observation group was treated with routine nitroglycerin therapy combined with Shiquan Dabu Decoction.The therapeutic effect of the two groups after one week of treatment was observed. Results: The total effective rate in the observation group was 92.73%, which was significantly higher than that of the control group(78.18%), and the difference between the two groups was statistically significant(χ²=4.681, P<0.05). The HR level of the observation group[(82.5±6.5)times/min] was significantly lower than that of the control group[(102.6±3.9)times/min](t=19.655, P<0.01). The levels of SBP[(116.5±6.4)mmHg]and SpO₂[(95.2±1.6)%] in the observation group were significantly higher than those in the control group[(108.8±5.2)mmHg, (92.5±1.2)%], there were statistically significant differences between the two groups(t=6.925, 10.012, all P<0.01). The incidence of adverse reaction in the observation group was 10.91%, which was higher than that in the control group(3.64%), but there was no statistically significant difference (χ²=2.157, P>0.05). Conclusion For patients with heart failure after acute myocardial infarction, the combination of traditional Chinese medicine Shiquan Dabu Decoction in clinical routine treatment has better effect and is worthy of popularizing.