Aim To study the anti-stress depression effect of Jiaweisinisan(JWSNS)and it's mechanism of N-methyl-D-aspartate(NMDA)receptor channel in hippocampus.Methods Chronic mild unpredictable stress(CMUS)was adopted to establish the rat depres-sion model.Before and after model establishing,the sucrose consumptions and the weight of rats were detected.TTC dyeing of hippocampus brain slices ex vivo were used to detect the situation of hippocampus neuron damage and the protective effect of serum containing components of JWSNS.The opening probability and the average opening time of NMDA receptor channels were detected by attach on cell patch clamp,the Ca2+ concentrations in single cell of hippocampus neurons were detected by Tillvis ION software.Results CMUS could decrease the sucrose preference and the weights of rats(P

Objective To evaluate the efficacy of comprehensive treatment for liver cancer recurrence and metastasis after liver transplantation, and investigate the risk factors affecting the lifespan of patients with liver cancer recurrence and metastasis. Methods Of 29 patients with liver cancer recurrence and metastasis after liver transplantation, 11 patients in the comprehensive treatment group were treated by TACE, microwave coagulation, radiotherapy or hepatectomy, and the remaining 18 patients were classified into chemotherapy group. The differences in efficacy between the 2 treatment modalities were compared, and the factors influencing the patients' lifespan were analyzed. Results Compared with patients in the chemotherapy group, patients in the comprehensive treatment group had significantly longer lifespan after liver cancer recurrence and metastasis (t = 5. 617, P < 0.01). TNM staging, pathological classification, time of postoperative recurrence and metastasis and treatment method were the factors that influence the lifespan of patients with liver cancer recurrence and metastasis after liver transplantation (t =2.843, 3.061,22.781,5.617, P <0.01). Conclusions Comprehensive treatment could prolong the lifespan of patients with liver cancer recurrence and metastasis after liver transplantation. The efficacy of comprehensive treatment is superior to that of the chemotherapy.

BACKGROUND:Shujin Jiannao Prescription is an empirical formula for the treatment of cerebral palsy in Dongzhimen Hospital,Beijing University of Chinese Medicine,with clear clinical efficacy,but the specific mechanism needs to be elucidated. OBJECTIVE:To explore the possible mechanism of Shujin Jiannao Prescription in treating cerebral palsy. METHODS:Sixty-four 7-day-old Sprague-Dawley rats were randomly divided into a normal group(n=12)and a model group(n=52).An animal model was established by the Rice-Vannucci method.After successful modeling,52 model rats were randomly divided into control model group(n=12),minocycline group,and the low-,medium-,and high-dose groups of the Shujin Jiannao Prescription(n=10 per group).Rats in the minocycline group were given 40 mg/kg·d minocycline by gavage;rats in the low-,medium,and high-dose groups were given 4,8,and 16 g/kg·d Shujin Jiannao Prescription granules by gavage,respectively;and rats in the normal group and control model group were given an equal dose of normal saline by gavage.Medication in each group was given once a day for 1 week.The rats in each group were evaluated behaviorally using suspension test,abnormal involuntary movement score,and Bederson score.The pathological changes of the cerebral cortex were observed by hematoxylin-eosin staining.The levels of tumor necrosis factor α,interleukin 1β,and interleukin 10 in the cerebral cortex were determined using ELISA.The positive expressions of Janus kinase 2(JAK2),phosphorylated Janus kinase 2(p-JAK2),phosphorylated signal transducer and activator of transcription 3(p-STAT3)in the cerebral cortex were detected using immunohistochemistry.The protein expression levels of JAK2,p-JAK2,and p-STAT3 were detected using western blot. RESULTS AND CONCLUSION:Compared with the normal group,the suspension test score and involuntary movement score were decreased in the control model group(P＜0.01 or P＜0.05).The pathological results showed structural disruption of nerve cells,formation of large numbers of vacuoles,cell swelling,and increased intercellular space in the control model group.In addition,the expressions of tumor necrosis factor α and interleukin 1β in the cerebral cortex were significantly increased(P＜0.01),the expression of interleukin 10 was decreased(P＜0.05),and the protein expressions of JAK2,p-JAK2,and p-STAT3 in the cerebral cortex were significantly increased(P＜0.01)in the control model group compared with the normal group.Compared with the model group,minocycline and Shujin Jiannao Prescription at each dose could improve the behavioral indexes of rats(P＜0.01 or P＜0.05)and ischemic-hypoxic pathological changes were attenuated,with only a small amount of necrotic nerve cells and a few vacuoles,and reduced intercellular space.Moreover,the expressions of tumor necrosis factor α and interleukin 1β in the cerebral cortex were decreased in each drug group compared with the control model group(P＜0.05),while the protein expressions of JAK2,p-JAK2,and p-STAT3 in the cerebral cortex were significantly decreased(P＜0.01).The most obvious improvement was observed in the high-dose Shujin Jiannao Prescription group.To conclude,Shujin Jiannao Prescription can inhibit inflammation in the cerebral cortex of rats with hypoxic-ischemic brain injury.The mechanism may be related to the regulation of the JAK2/STAT3 signaling pathway.

UHRF2 is a ubiquitin-protein ligase E3 that regulates cell cycle, genomic stability and epigenetics. We conducted a co-immunoprecipitation assay and found that TIP60 and HDAC1 interact with UHRF2. We previously demonstrated that UHRF2 regulated H3K9ac and H3K14ac differentially in normal and cancer cells. However, the accurate signal transduction mechanisms were not clear. In this study, we found that TIP60 acted downstream of UHRF2 to regulate H3K9ac and H3K14ac expression. TIP60 is stabilized in normal cells by UHRF2 ubiquitination. However, TIP60 is destabilized in cancer cells. Depletion or inhibition of TIP60 disrupts the regulatory relationship between UHRF2, H3K9ac and H3K14ac. In summary, the findings suggest that UHRF2 mediated the post-translational modification of histones and the initiation and progression of cancer.
Cell Line ; Histone Acetyltransferases ; genetics ; metabolism ; Histones ; genetics ; metabolism ; Humans ; Lysine Acetyltransferase 5 ; Neoplasm Proteins ; genetics ; metabolism ; Neoplasms ; genetics ; metabolism ; RING Finger Domains ; Ubiquitin-Protein Ligases ; genetics ; metabolism ; Ubiquitination