Heart failure is a complex clinical syndrome,and impaired filling or ejection disorders result from any ventricular structure or dysfunction can cause heart failure.The prevalence of heart failure in adult populations in developed countries has reached 1% to 2%,while the prevalence in elderly people over 70 years of age has increased to ≥ 10%. With the population aging and the prevalence of coronary heart disease increased, the prevalence of heart failure has increased,becoming a disable and fatal disease.The changes of the central nervous system hormones such as renin-angiotensin system (RAS),inflammatory cytokines (proinflammatory cytokines,PIC),and reactive oxygen species (ROS)may be closely related to increased central activity in heart failure,which can significantly alter the activities of peripheral sympathetic nerves. Constant sympathetic nervous activity is an important cause of development of heart failure,so reducing the sympathetic excitability of heart failure is regarded as one of the focuses of treatment and research.This paper focuses on the influence of central neurohormone on heart failure and possible central mechanism.

AIM: The present study was undertaken to investigate the effect of angiotensin II (AngⅡ) on expression of MMP-9 in THP-1 macrophages. METHODS: Macrophages converted from THP-1 monocytes by incubating with PMA (0.1 μmol/L) for 48 h were divided into PMA group; PMA+AngⅡ group (10-7mol/L, 1 h); PMA+AngⅡ+PDTC group (10 μmol/L, 30 min) and PDTC group. Western blotting was used to detect the MMP-9 and phosphorylation of NF-κB p65, and the expression of MMP-9 mRNA in THP-1 macrophages was measured by RT-PCR.RESULTS: Compared to control group, the expression of MMP-9 (1.06±0.11, P<0.05) and phosphorylation of NF-κB p65 (1.02±0.10, P<0.05) in THP-1 macrophages were expressed when treated with AngⅡ (10-7mol/L); and the expression of MMP-9 mRNA were upregulated (1.22±0.08, P<0.05). However, NF-κB inhibitor PDTC reduced the NF-κB p65 (0.99±0.12, P<0.01) and MMP-9 (1.04±0.14, P<0.01) expressions and decreased the expression of MMP-9 mRNA (0.90±0.06,P<0.01). CONCLUSION: NF-κB signaling pathway contributes to the expression of MMP-9 in THP-1 macrophage induced by AngⅡ.

ABSTRACT:Hypertension,the first risk factor for stroke and coronary heart disease in the Chinese population, seriously endangers people’s health.At present,China has more than 270 million people with hypertension and an annual increase rate of 1 0 million people.Then how to improve prevention and treatment of hypertension has become an urgent need to solve major medical and social problems.In the past,research on hypertension mainly focused on the peripheral area,while recent research has shown that the central regulation plays an important role in the development of hypertension. Hypothalamic paraventricular nucleus (PVN ), which plays a key role in maintaining cardiovascular activity, can directly control the sympathetic preganglionic neurons and regulate peripheral sympathetic nerve activity,thus being closely related to the development of hypertension.Research in recent years shows that the comprehensive effects of proinflammatory cytokines (PIC ),reactive oxygen species (ROS),renin-angiotensin system (RAS),neurotransmitter (NT)and nuclear factorκB (NF-κB)are involved in the pathogenesis of hypertension.However,it is unclear how these neurohormones in PVN are activated,how they interact with each other and what role they play in the regulatory mechanism of hypertension.Therefore,the key focus of this research is to explore the impact of activated neurohormones in PVN on hypertension.This study will provide new content for the study on hypertension.

BACKGROUND:Adipose-derived stem cel s have a wide variety of sources and strong proliferation ability, which are easy to access and simple to culture. Therefore, adipose-derived stem cel s that are secondary to bone marrow mesenchymal stem cel s are expected to become the most promising seed cel s for bone tissue engineering.
OBJECTIVE:To explore the feasibility of rabbit adipose-derived stem cel s with demineralized bone matrix to repair ulna defects.
METHODS:Ulna defect model was made in rabbits. Demineralized bone matrix was implanted into the right defect region as control group. After osteogenic induction, rabbit adipose-derived stem cel s/demineralized bone matrix composite was implanted into the left defect region as experimental group. At 12 weeks after implantation, defect tissues were taken for CT scanning and histological detection.
RESULTS AND CONCLUSION:CT results showed that there was unclear boundary between the broken ends of fractured bone and the composite material in the experimental group, and paral el cal uses out of the broken end could be seen. In the control group, the broken end was clearly seen and no cal us occurred continuously. Fibers were connected at the defect site, and no new bone occurred. Histological findings showed that typical regenerated bone tissues were seen in the experimental group with osteocytes, bone lacunae and bone trabeculae;there were more osteocytes and bone lacunae, but bone trabecula was only seen in a part of bone defects;a few of col agens interlarded the regenerated bone tissues. In the control group, the residual of demineralized bone matrix was seen as wel as some col agenous fibers, and periosteal bone formed a little, but no large amount of regenerated osteoid tissues were found. These findings indicate that under osteogenic induction, rabbit adipose-derived stem cel s combined with demineralized bone matrix are feasible to repair ulna defects.

AIM: To observe the expression of corticotropin releasing hormone (CRH) within the paraventricular nucleus of hypothalamus (PVN) and to explore the relationship between the activated CRH-containing neurons and sympathetic activity in rats with heart failure (HF).METHODS: Healthy male Sprague-Dawley (SD) rats were subjected to coronary artery ligation to induce HF, and chronic intracerebroventricular (ICV) infusion was performed by osmotic pump for 4 weeks.The rats in sham group and HF group were given vehicle (VEH;artificial cerebrospinal fluid 0.25 μL/h).The rats in HF plus treatment group were treated with CRH competitive inhibitor αh-CRH (15 mg/h).Meanwhile, the Lewis rats and Fischer 344 rats for control study also underwent coronary ligation to induce HF or sham surgery.After 4 weeks, left ventricular end-diastolic pressure (LVEDP) and maximum positive/negative change in pressure over time (±dp/dtmax) were determined.The right ventricular-to-body weight (RV/BW) and lung-to-body weight (lung/BW) ratios were calculated.The renal sympathetic nerve activity (RSNA) was recorded and the plasma norepinephrine (NE) level was measured.The expression of CRH in the PVN combined with the plasma adrenocorticotrophic hormone (ACTH) levels were measured.RESULTS: Compared with the sham-SD rats, the HF-SD rats had a greater number of CRH positive neurons in the PVN (accordingly the plasma ACTH levels were increased), accompanied by decreased ±dp/dtmax and increased RSNA, plasma NE, LVEDP, lung/BW and RV/BW.However, ICV treatment with αh-CRH attenuated these changes in the HF-SD rats (P<0.05).Compared with the sham-Fisher 344 rats, the HF-Fisher 344 rats also had a greater number of CRH positive neurons in the PVN (accordingly the plasma ACTH levels were increased).In addition, they had significantly increased RSNA and plasma NE level, higher LVEDP, RV/BW and lung/BW, and lower ±dp/dtmax (P<0.05).Compared with the SHAM-Lewis rats, the HF-Lewis rats had not significantly changed in the above parameters.CONCLUSION: In CHF, the CRH-containing neurons in PVN are activated, thus aggravating cardiac function by increasing sympathoexcitation.

0.05). ALP activity of the cells on deproteinized bone was higher than that on decalcified bone(P

AIM:The present study was undertaken to investigate the effect of angiotensin II (AngⅡ) on expression of MMP-9 in THP-1 macrophages. METHODS:Macrophages converted from THP-1 monocytes by incubating with PMA (0.1 ?mol/L) for 48 h were divided into PMA group; PMA+AngⅡ group (10-7mol/L,1 h); PMA+AngⅡ+PDTC group (10 ?mol/L,30 min) and PDTC group. Western blotting was used to detect the MMP-9 and phosphorylation of NF-?B p65,and the expression of MMP-9 mRNA in THP-1 macrophages was measured by RT-PCR.RESULTS:Compared to control group,the expression of MMP-9 (1.06?0.11,P

AIM: To investigate the effect of Ganoderma lucidum spores powder on the expression of insulin-like growth factor-1 (IGF-1), nuclear factor-?B (NF-?B) and apoptosis of nerve cells in rats with epilepsy established by pentetrazole. METHODS: The sub-eclampsia dosage of pentetrazole (PTZ) was used to make epilepsy model. Ganoderma lucidum spores powder group was given from stomach. The enduring time and latent period were recorded. The immune reactivity of IGF-1, NF-?B/P65 and apoptosis of nerve cells were measured with immunohistochemical staining and TUNEL method. RESULTS: In high power sight (?400), there were much more apoptosis cells in hippocampus and brain cortex of model group (18.80?2.13, 16.87?2.00) than those in control group (0.97?0.52, 0.58?0.25). The expressions of IGF-1, NF-?B in model group were higher than those in control group. Compared with model group, the latent period of Ganoderma lucidum spores powder group at the 17th, 21th, 25th days were longer (P

0.05).CONCLUSION:Ang-(1-7) inhibits the secretion of MCP-1 and ICAM-1 in cultured HUVEC in a concentration dependent matter induced by AngⅡ. The inhibitory effect of Ang-(1-7) may be through its specific receptor.

AIM:To investigate the protective effect of losartan(Los) on apoptosis of H9c2 cells induced by isoprenaline(ISO),and to discover its related mechanism.METHODS:H9c2 cells cultured on plastic plates were divided into control,ISO,ISO+Los,ISO+Los+LY294002 and DMSO groups.Cell apoptosis was evaluated by flow cytometery and agarose gel electrophoresis.The mRNA levels of bax,bcl-2 and caspase-9 were detected by RT-PCR and the expressions of phosphorylated and total Akt(p-Akt and t-Akt) were assessed by Western blotting.The cAMP was measured by radioimmunoassay.RESULTS:ISO at concentration of 10 ?mol/L induced apoptosis of H9c2 with an increase in bax/bcl-2,caspase-9 and cAMP.Addition of 10 ?mol/L losartan inhibited apoptosis obviously with a decrease in bax/bcl-2,caspase-9 and cAMP.A significant increase in p-Akt was observed,and its protein level was elevated.LY294002 at concentration of 1 ?mol/L abolished the protective effects of losartan on ISO-induced apoptosis in H9c2 cells.CONCLUSION:ISO might induce H9c2 cell apoptosis through stimulation of ?-adrenergic receptor(?-AR).Los inhibits downstream signaling of ?-AR,and promotes the activation of Akt.Subsequently it might attenuate the apoptosis induced by ?-adrenergic stimulation of ISO.