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OBJECTIVE To investigate the effect of extract of St.John's wort tablets (ESJWT) on post-traumatic stress disorder (PTSD) in a mouse model and explore possible avenues for the treat-ment of PTSD.METHODS Forty-eight C57BL/6 male mice were randomly divided into 4 groups:normal control group, model group, sertraline and ESJWT treatment groups, with 12 mice in each group. Except the normal control group, all the mice were treated with fifteen intermittent inescapable foot-shocks (intensity:0.8 mA;interval:10 s;duration:10 s)for 2 d.Sertraline 15 mg·kg-1and ESJWT 25 mg·kg-1 were ig given one hour before foot-shocks repectively,once a day,for 18 d.Then,contextual freezing and fecal pellet were tested on the 3rd,8thand 15thdays.In addition,open field test,elevated plus maze test and staircase test were performed on the 16th, 17thand18thdays, respectively. Here, the day mice were subjected to short foot-shocks was defined as the 1stday.The serum contents of norepinephrine (NE) and 5-hydroxytryptamine (5-HT) were evaluated using ELISA after behavior tests. RESULTS Compared with normal control group, the freezing time and the number of fecal pellet in model group were significantly increased(P<0.01).Meanwhile,the time and number of entries into the central open field and open arm were decreased(P<0.01).The above experiments indicated that the mouse model of PTSD was established successfully. Compared with model group, both sertraline and ESJWT extract showed anti-PTSD effect, with the decreased percentage of freezing time (P<0.05, P<0.01). ESJWT extract treatment also reduced the amount of fecal pellet(P<0.01).However,no significant changes of the contents of NE and 5-HT in any group were seen.CONCLUSION ESJWT has anti-PTSD effect in the mouse model,which might be used for the treatment of PTSD.
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Post-traumatic stress disorder (PTSD) is a mental disorder that develops after individual exposure to one or more traumatic events.Natural disasters and war are the major primers of PTSD.Tt is affracting more attention due to the high prevalence in war veterans and natural disasters.The risk factors range from gender,environment to physiology.Hypothalamic-pituitary-adrenal (HPA) axis plays an important role in stress reaction and dysfunction of HPA axis leads to disorder of neuroendocrine.In addition,chronic inflammation,including adaptive and innate immune response disorder,has been reported in many PTSD studies.Neural imaging studies have found that there are significant changes in the brain structure and neural circuits of PTSD patients.However,the biological mechanism underlying PTSD is largely unknown.Currently,based on the clinic symptoms of PTSD patients,anti-depression and anxiety drugs are the first choice for treatment,but the outcomes are diverse.Some potential therapeutic drugs or avenues that are derived from the identified targets are still under investigation.In this review,we overview and summarize the biological changes of PTSD,focusing on disorder of neuroendocrine,chronic inflammation,brain structure and circuits changes and therapeutic strategies in clinical and preclinical trials.This review aims to will provide new ideas for revelation of PTSD mechanisms and develop novel therapies.
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<p><b>OBJECTIVE</b>This study aimed to investigate the genetic background of mitochondrial genes in young patients with Coronary heart disease (CHD) to provide a foundation for the early prevention of young patients with CHD.</p><p><b>METHODS</b>115 cases of young (⋜ 45 years) CHD Chinese Han patients (case group), 100 cases of older (> 45 years) Chinese Han CHD patients (experimental group) hospitalized and 100 cases of healthy people through physical examination (control group) at the General Hospital of PLA between January 2014 and December 2015 were selected. General information, clinical assessment, pedigree analysis, and mitochondrial full sequence scanning were performed. The pedigrees of one patient harbouring the C5263T mutation were recruited. Mitochondrial functional analysis including cellular reactive oxygen species (ROS) levels and mitochondrial membrane potential (MMP) were performed on pedigrees with the C5263T mutation (mutation group) and without the mutation (non-mutation group).</p><p><b>RESULTS</b>The differences in biochemical tests (P > 0.05) between the case group and experimental group were not significant. The C5263T single-nucleotide mutation of the mitochondrial ND2 gene was observed in 2 young CHD patients in the case group. The premature CHD of these 2 patients followed a pattern of maternal inheritance. The mutation group (I1, II2) had higher ROS levels (4750.82 ± 1045.55 vs. 3888.58 ± 487.60, P = 0.022) and lower MMP levels (P = 0.045) than the non-mutation group (II1, III1, III2).</p><p><b>CONCLUSION</b>We speculated that the mitochondrial C5263T mutation might be associated with the occurrence CHD in Chinese Han young people.</p>