Fibrosis is an important pathoIogicaI change in a variety of diseases and with compIicated causes. Fibrosis diseases in different organs have different causes,but the common manifestations of fibrobIast are proIiferation and coIIagen deposition that couId eventuaIIy Iead to normaI tissue damage and Ioss of function. Fibrosis in such important organs as the heart or Iung couId be Iife-threatening. There are different reguIating factors and drugs to fibrosis. Chinese medicine treatment is stiII the main method cIinicaIIy for Iiver fibrosis. Because there is no effective cure for puImonary fibrosis,treatment focuses on anti-infIammation by aIIeviating Iesion and improving kidney function. Despite the tremendous progress in fibrosis treatment,there is stiII a Iack of targeted drugs that couId cure a specific disease in a specific area. With the deveIopment of gene technoIogy,gene therapy wiII become an important treatment for this disease. This paper introduces anti-myocardiaI fibrosis drugs according to the mechanism.

AIM: To observe the protective effect of heat stress preconditioning on endothelial cells under anoxia and explore its mechanism. METHODS: The endothelial cells were divided into 4 groups: (1) anoxia; (2) heat stress; (3) heat stress preconditioning + hypoxia; (4) control. LDH activity was measrued by using Automatic Biochemistry Analysis-Meter. Cell death rate was determined by trypan blue, NO production was tested by measuring NO - 2/NO - 3 content in cellular culture medium by using Griess assay. RESULTS: LDH release and cell death rate of the anoxia endothelial cells significantly increased compared with control; 39℃ heat stress preconditioning reduced those increment by 29、47%, 33.67% respectively. 41℃ heat stress preconditioning has no protection against the anoxia-induced injury in endothelial cells. The NO production in anoxic endothelial cells decreased markedly. 39℃ heat stress preconditioning induced the increase in NO production in endothelial cells, but 41℃ heat stress preconditioning made the NOS activity decrease. The NO production was correlated negatively with LDH release and cell death rate in anoxic endothelial cells. CONCLUSION: The heat stress preconditioning within the limits can protect the endothelial cells from anoxia injury. The increase in NO in endothelial cells may play an important role in the mechanism of the protective effect.

Chronic stress can induce hippocampus injury such as neuron loss, dendrite atrophy, but its mechanism and molecular basis remain unclear up to now. To understand the molecular mechanism on protein level and find the crucial proteins which correlated with chronic stress-induced injury, two-dimensional electrophoresis was applied to separate the hippocampal total proteins of control group and restraint stressed rats, then the differential expressed proteins were detected by image analysis and identified by matrix assisted laser desorption /ionization time of flight mass spectrometry (MALDI-TOF-MS) as well as database searching. Moreover, the 2-DE results were verified on the mRNA level by semi-quantitative RT-PCR. The hippocampal 2-DE map with high resolution and good reproducibility of control and stress group rats were obtained. Fourteen differentially expressed protein spots were detected and eleven proteins were successfully identified, most of these proteins were involved in the process of energy metabolism and signal transduction. These results provide a clue for elucidating the mechanism of chronic stress-induced hippocampal injury and are useful for elevating the adaptability to stress.

AIM: To investigate the effects of stress on the opening of mitochondrial membrane permeability pore (PTP) in rat heart and explore the possible molecular mechanism underlying PTP opening. METHODS: Stress animal model was established. After strained for differnet time, all rats were killed and PTP opening degree were examined by spectrophotometer. Bcl-2, Bax expression levels were determined by Western blot. RESULTS: Stress induced PTP opning, Bcl-2 expression inhibition and Bax level elevation in myocardial mitochondria. CONCLUSION: PTP opening was the important mitochondrial mechanism of stress-induced heart injury. Decrease in Bcl-2 expression and increase of Bax level may be an important molecular basis for PTP opening.

Objective To investigate the anti-fatigue activity of fermented grain-containing blueberry anthocyanins ( LANHE,LH) in mice.Methods Experiments were conducted in two phases .In the first phase , forty mice were randomly divided into four groups:control group(distilled water,dw) and three LH administration groups (8.75,17.5 and 35.08 ml/kg body mass).In the second phase, mice were randomly divided into two groups:high-dose LH group (35.08 ml/kg body mass) and control group (dw 35.08 ml/kg body mass).After four weeks, a forced swimming test was performed and the biochemical parameters related to fatigue were examined .Results and Conclusion The administration groups showed a significant increase of swimming time to exhaustion compared with the control group , especially the high-dose group ( P<0.001).There was no significant change in the blood lactate between the two groups , but at 20 min after swimming, the lactic acid(LA) contents of the high-dose group were lower than in the control group (P>0.05).LH could significantly increase the liver glycogen contents and decrease the serum contents (P<0.05).These data indicate that LH has anti-fatigue activity and can elevate the exercise tolerance in mice .

Objective To systematially observe the different patterns and leves of military stress on modified multitle-platform method the level of stress-related hormones in rats .Methods A sleep deprivation model was established by water environment modified multiple-platform method(MMPM).A restraint stress model was established by self-made bondage cage.Chronic unpredictable mild stress ( CUMS) model was established by action control , cage damp, cage tilt, night lightening, water and food fasting , empty bottles stimulation and group feeding methods .Cortisol, catecholamines and 5-HT levels were detected to observe the different military stress loads and modes on the level of stress hormones .Results The level of serum cortisol increased significantly ( P <0.05 ) after 5 days of sleep deprivation .The level of serum catecholamines increased significantly (P<0.05) after 1 day of sleep deprivation.The cortisol concentration increased and the level of 5-HT decreased in serum after 4 weeks CUMS.The level of catecholamines increased significantly (P<0.05) after 2-8 weeks of CUMS, increased significantly (P<0.05) after 1 week of restraint stress , and returned to normal after 3-4 weeks of restraint stress .The level of serum cortisol increased significantly after 3 -4 weeks of restraint stress . Conclusion Cortisol levels gradually increased with the level of stress in different military stress modes , which can serve as an index to evaluate the level of different stress modes .

Objective To study the possibility of the plasma level of heat shock protein 70(HSP70) being used as a bi-ological marker of military stress .Methods Soldiers who returned from a 6-month-navigation were chosen as subjects , the HSP70 level of plasma was measured with the ELISA assay and stress questionnaires and Self -rated Health Measurement Scale (SRHMS) were used to measure the stress level .Results The soldiers′plasma level of HSP70 was 31.40%higher than that of the control .The stress questionnaire indicatesd that the level of thinking and anxiety , negative mood and somat-ic symptoms were higher than normal .The SRHMS indicated that the level of physiological health ,mental health and social health was lower than normal .The plasma level of HSP70 was associated with the level of military stress .Conclusion The plasma level of HSP70 may be used as an important predictor of military stress .It can predict the level of military stress injury.

Objective To investigate the effect of MALAT1 expressions on cell proliferation and apoptosis in astrocytes by regulating mitogen-activated protein kinase(MAPK)/extracellular signal-regulated kinase(ERK1,2)pathway.Methods The MALAT1 gene was knocked down and over-expressed in C8-D1A cells by lentiviral and plasmid vectors,respectively.The expressions of MALAT1,cell proliferation-related markers(Ki67,MCM2,PCNA)and apoptosis-related proteins(Caspase-3,Bax,Bcl-2)were detected by quantitative real-time polymerase chain reaction(qPCR).CCK-8 assay and flow cytometry were used for cell proliferation and apoptosis in C8-D1A cells.Immunofluorescence was adopted to detect the protein expressions of Caspase-3 and Ki67.Western blotting was used to detect the protein expressions of Caspase-3,Bax,Bcl-2,ERK1/2,p-ERK1/2,p38MAPK and p-p38MAPK.Results Compared with the control group,over-expressed MALAT1 inhibited cell proliferation and induced cell apoptosis in C8-D1A cells while the knockdown of MALAT1 significantly enhanced cell proliferation and anti-apoptotic ability in C8-D1A cells.The proportion of C8-D1A cells in G0/G1-phase and G2/M-phase was higher than in the control group as evidenced by flow cytometry,but was lower in S-phase.Meanwhile,data showed that Caspase-3 was increased while p-ERK1/2 was decreased in terms of protein levels.The mRNA expressions of Ki67 and PCNA were decreased.After knockdown of MALAT1,the proportion of C8-D1A cells in S-phase was higher,but was lower in G2/M-phase.The protein expressions of Caspase-3 and Bax decreased while those of p-ERK1/2 and p-p38MAPK increased.The mRNA expressions of Ki67,MCM2 and PCNA were increased.The differences were all statistically significant(P＜0.05).Conclusion MALAT1 promotes astrocyte apoptosis and inhibits proliferation by regulating the MAPK/ERK1,2 signaling pathway.