Objective To investigate the morphological changes during the development and aging of C57/BL6 mouse hippocampus.Methods Serial sections and stereology were used to quantitatively analyze the development of C57/BL6 mouse hippocampus at different growth stages.Results Hippocampus primordium first appeared at embryonic day 12(E12d).A "C" outline could be seen in the pyramidal layer of Ammon's horn(CA),and the extra-arm's blanket of the dentate gyrus(DG)'s granular layer formed at E18d.After birth,CA developed and maturated gradually.The blanket of DG's granular layer formed at postnatal day 7(P7d).At P21d,the inner arm's thickness of DG's granular layer was equal to that of the extra-arm,and the subgranular layer was present until month 15(15M).The increase of the volume of hippocampus,CA,DG and CA's layers was slow before P7,became fast from P7d to P14d and slowed down again after P14d,but became stable after 3M.Conclusion Mouse hippocampus is formed at E12 and becomes basically mature at month 3.The volume of aging mouse hippocampus has no obvious changes.

Anthracyclines, which include doxorubicin, epirubicin, daunorubicin, and aclarubicin, are widely used chemotherapeu-tic agents for treating hematologic and solid tumors, such as acute leukemia, lymphoma, breast cancer, gastric cancer, soft tissue sarco-mas, and ovarian cancer. Anthracyclines can be combined with other chemotherapeutics and molecular targeted drugs for cancer treat-ment. The combination of anthracyclines with other chemotherapeutic drugs is usually the standard of first-line treatment. Anthracy-clines are efficacious and potent agents with broad antitumor effects. However, these drugs may cause adverse reactions, such as hair loss, myelotoxicity, and cardiotoxicity. Hematopoietic stimulating factors, such as granulocyte colony-stimulating factor, erythropoietin, and thrombopoietin, can be used to control myelotoxicity. However, cardiotoxicity is the most serious anthracycline side effect. Clinical study results and practical observations indicate that the anthracycline cardiotoxicity is usually progressive and irreversible, especially after the first use of the drug, which may particularly cause heart damage. Therefore, the early detection and prevention of anthracy-cline-induced cardiotoxicity are important and have already gained considerable attention in clinical applications. Relevant experts from the China Society of Clinical Oncology and Hematology Branch of the Chinese Medical Association prepared the guidelines for the pre-vention and cure of anthracycline-induced cardiotoxicity in 2013. The authors reviewed the effective drugs currently used to prevent and cure anthracycline cardiotoxicity.

Objective To dynamically observe the effect of compound decotion on changes of Na+-K+-ATPase,Ca2+-ATPase activity,intracellular free Ca2+ contents and CaM expression jn bomogenate and mitochondria of rat brain tissues after traumatic brain injury(TBI)and investigate the molecular mechanism of neuroprotective effect of compound decotion.Methods Rat TBI models were made and divided into sham operation group,TBI group and compound decotion treatment group(treated with comof normal saline,twice per day for seven days.Rats were sacrificed at 24 h,72 h and 1 week after injury to dynamically observe activities of Na+-K+-ATPase and Ca2+-ATPase in bomogenate and mitochondria of rat brain tissues,concentration of free Ca2+ in neurocytes and expression change of CaM in brain tissues.Results The activities of Na+-K+-ATP ageand Ca2+-ATPase in homogenates and mitochondria of brain tissues markedly decreased at different time point and increased gradually after 72 hours in TBI group but wag still lower than that of sham operation group at one week after injury.However,compound decotion could significantly enhance the activities of Na+-K+-ATPageand Ca2+-ATPage(P＜0.05).In TBI group,concentration of free Ca2+ in neurocytes and CaM expression in brain tissues were elevated at different degrees at different time point and reached peak at 24 hours after injury but still lower than that of sham operation group at 72 hours.While concentration of free Ca2+ in neurocytes and CaM expression in brain tissues were significantly lower than those of TBI group at different time point(P＜0.05).Conclusions The neuroprotective effect of compound decotion may be related to its role in increasing activities of Na+-K+-ATPase and Ca2+-ATPase to facilitate cellular metabolism and decreasing concentration of free Ca2+ in neurocytes and CaM expression in brain tissues to mitigate secondary brain injury induced by Ca2+ over load.

Aim To investigate the antiepileptic activity of alpha-asarone in three epilepsy models.Methods The MES mice,MST mice and Lithium-pilocarpine rats were divided randomly and respectively into groups each containing 20 animals(?-asarone groups,AED groups and normal control group).Different doses of alpha-asarone were administered to mice/rats in advance in alpha-asarone treated groups,one group received only saline,while the other groups received antiepileptic drug as a reference standard,2 times per day for 28 days.The seizure severity score,seizure latency and total number of animals with seizures were noted to observe whether alpha-asarone had anticonvulsant effect or not in three epilepsy models.Results Alpha-asarone possessed excellent anticonvulsant effect in MES and MST and lithium-pilocarpine models. It significantly decreased the seizure incidence 40%~100% in the MES models and 50%~90% in MST models,and 40%~80% in the Lithium-pilocarpine model. It significantly prolonged the seizure latency 70~180 s in MST mice and 4~15 min in Lithium-pilocarpine rats;It significantly reduced the seizure severity scores 1.96 in Lithium-pilocarpine rats.Conclusions Alpha-asarone had a positive antiepileptic activity.

Objective To investigate the effect and possible mechanisms of high mobility group box (HMGB) 1 on the proliferation of RSC-364 synoviocytes. Methods ① RSC-364 cells stimulated by 10 μg/L TNF-α and cells of the normal control groups were collected at 6, 12, 24 h respectively in vitro. HMGB1mRNA and protein was detected by reverse transcription polymerase chain reaction (RT-PCR) and immunocytochemistry (ICC); ②RSC-364 cells induced by 10 μg/L HMGB1 were collected in 6, 12, 24 h respectively, so did normal control group cells in vitro. The expression of signal transducer and activator of transcription (STAT) mRNA 1 was detected by RT-PCR. The expression of STATland SOCSI proteins were detected by ICC and flow cytometry analysis (FCM). The expression of PCNA was detected by ICC. Results ① Compared with the control group, TNF-α markedly up-regulated HMGBI mRNA at 6, 12, 24 h respectively [0.86, 0.92, 1.06 vs 0.70, P<0.01 ], as well as protein expression level. Positive signal of HMGB1 proteins was not only expressed in nuclear but also in cytoplasm after stimulation. ② Compared with normal group, HMGBI increased the expression of P-STAT1 mRNA and protein at 6, 12, 24 h respectively [0.30, 0.69, 1.05 vs 0.24, P<0.01 ] and [1.34±0.09，1.55±0.16，1.74±0.13 vs 1.00±0.15，P<0.01]. The expression of SOCSI protein increased significantly in HMGB1 group at 6 and 12 hours ( 1.43±0.10 vs 1.58±0.05), but it decreased at 24 hours (1.24±0.15). ③The expression of p-STATI protein was negatively correlated with that of SOCS1 protein. Conclusion HMGB1 appears to be an important mediator in the proliferation of RSC-364 cells, partly by up-regulating the expression and aetivity of p-STAT1.

Objective To investigate the correlation between NF-?B/COX-2 signal pathway and cell proliferation in diabetic nephropathy. Methods Uninephrectomized STZ-induced male Wister rats were used as animal model. Using immunohistochemistry to detect NF-?B and COX-2 protein expressions in diabetic kidneys at the 16th week. HKC were cultured separately in normal or high glucose medium for 24,48,72 h.The expression of NF-?B and COX-2 protein was detected by flow cytometry and the expression of PCNA was detected by immunocytochemical staining. Results 1 Volum of glomeruli, mesangial matrix, thickness of glomerular and tubular basement membrane increased in diabete group; 2 COX-2 were expressed in cytoplasm of tubules and glomeruli by immunohistochemistry. Compared with control group, the expression of COX-2 was higher; activated NF-?B expressed in nucli of both tubules and glomeruli, There was light stainings for in control group, while enhanced stainings were observed in DM, there was a positive correlation between NF-?B and COX-2.3 Compared with those in HKC cultured in the medium with normal level glucose, the stainings were strengthened for PCNA in HKC exposed to high glucose from 24 h. 4 By FCM, the expression of NF-?B and COX-2 in HKC cultured in high glucose medium was higherthan that in normal glucose medium; the expression of NF-?B and PCNA was positively correlated with the expression of COX-2. Conclusion Activating NF-?B and elevating the expression of COX-2 play an important role in regulating cell proliferation, which may be one of the injury mechanisms of the renal cells during diabetic nephropathy.

Objective To retrospectively analyze the effect of interventional embolization for hepatocelluar carcinoma (HCC) associated with arteriovenous shunting (AVS), and to discuss the factors influencing the therapeutic results. Methods The clinical data of 62 cases with HCC associated with AVS , who were treated with interventional chemoembolization , were retrospectively analyzed. Based on the type and extent of AVS identified by angiographic manifestations, appropriate obstruction of the shunt and Lipiodol chemoembolization of HCC were conducted. The curative effect of the shunt embolization was assessed by DSA at one or two months after the treatment. The relevant factors influencing the prognosis of embolization were analyzed by using univariate and multivariate Cox regression analysis methods. Results Of the 62 patients, arterioportal shunting (APS) was detected in 44, hepatic arterio-venous shunting (HAVS) in 11, APS together with HAVS in 4, and hepatic artery-pulmonary artery shunting (HAPAS) in 3. Re-examination with DSA was carried out in 53 patients at 1 - 2 months after the treatment , which showed that the shunting disappeared in 18 cases, obvious reduction of the shunt flow was seen in 19 cases, the lesion remained stable in 9 cases and the disease became worse in 7 cases. Univariate analysis indicated that the kind of embolic material and the presence of tumor thrombus could affect the obstructive result of the shunt , while multivariate Cox regression analysis showed that portal tumoral thrombus was an independent risk factor. The embolization effect of polyvinyl alcohol (PVA) particles and Lipiodol-ethanol mixture, used as the embolic agents, was better than that of gelatin sponge particles. Conclusion To ensure a successful interventional chemoembolization for HCC combined with AVS the procedure should be individualized according to the type and extent of the arteriovenous shunting. The type of embolic materials used for embolization can affect the results to a certain degree.

ObjectiveTo evaluate the technical feasibility of animal model of avascular necrosis of femoral head (ANFH)with transcatheter arterial embolization (TAE).MethodsTwenty experimental pigs were randomly divided into experimental group and control group (each n= 10).Experimental group:A 5F Cobra catheter was inserted into left femoral artery,and the feeding arteries of femoral head were superselectively inserted.The feeding arteries were embolismed through transcatheter arterial injecting the segments of silk measuring about 500μm.Control group:The arterial embolization was not performed,and the other treatment was identical to experimental group.The articulation of hip in all pigs underwent plain X-ray examination,CT and MR scanning 2 weeks and 4 weeks after treatment,respectively.Histological examination was made in 4 weeks to evaluate volume of bone trabecula (TBV) and percentage of bone lacuna (PBL) at unit area under microscope.The data were compared between the two groups.Results In experimental group,CT and MRI showed swolling in hip soft tissue and high T1 in hip joint cavity,while no obvious abnormalities were found in plain X-ray film 2 weeks after feeding arteries were embolized.Four weeks after feeding arteries embolization,plain X-ray film,CT and MR showed typical necrosis of femoral head in the experimental group,while no obvious abnormalities were found in control group.The histology examination revealed there were obvious karyopyknosis and anachromasis in the bone cells.The quantity of bone cells decreased obviously or disappeared.PBL increased and TBV decreased significantly compared with those of control group (P＜0.05).ConclusionThe animal model of ANFH in pigs can be induced by TAE.It can preferably mimic the pathological situation of ANFH.

AIM:To observe the protective effect of allitridi on hippocampal neuron of rats with cerebral ischemia-reperfusion (I/R) injury and to investigate its effects on P53 expression in hippocampus.METHODS: The global cerebral ischemia-reperfusion models were established by 4-vessel occlusion. Allitridi at doses of 10, 20 or 30 mg/kg was injected through rat’s tail vein, half dose at 30 min before brain ischemia and another half dose at 10 min after reperfusion were injected, respectively. The hippocampus of rat was removed 24 h after reperfusion. Toluidine blue staining was applied to estimate morphologic changes. Flow cytometry was used to evaluate neuronal apoptosis rate of hippocampus. Immunohistochemistry was used to observe the expression of P53 protein.RESULTS: Compared with sham group, survival neuronal density in I/R group was significantly depressed. The rate of neuronal apoptosis and the expression of P53 protein were significantly increased. Allitridi significantly increased the number of survival neurons in hippocampus compared to I/R group. Meanwhile, allitridi remarkably inhibited the rate of neuronal apoptosis and the expression of P53 protein.CONCLUSION: Allitridi has protective role against brain ischemia reperfusion injury. The mechanism may be involved in blocking P53 protein expression in hippocampus of rats with ischemia-reperfusion.