OBJECTIVES: To explore the mechanism of Qingda Granules (QDG) for alleviating brain damage in spontaneously hypertensive rats (SHRs). METHODS: Twelve 5-week-old SHRs were randomized into SHR control group and SHR+QDG group treated with QDG by gavage at the daily dose of 0.9 g/kg for 12 weeks. The control rats, along with 6 age-matched WKY rats, were treated with saline only. Blood pressure changes of the rats were monitored, and pathologies and neuronal apoptosis in the cerebral cortex were examined with HE staining and TUNEL staining. Cerebral cortical expressions of miR-124 and STAT3 mRNA were detected using RT-qPCR, and the protein expressions of NeuN, STAT3, Bcl-2, Bax, and cleaved caspase-3 were detected with immunohistochemistry and Western blotting. In a HT22 cell model of oxygen and glucose deprivation/reoxygenation (OGD/R), the effects of QDG on cell viability and apoptosis, expressions of miR-124 and STAT3 mRNA, and protein expressions of STAT3, Bcl-2, Bax, and cleaved caspase-3 were evaluated using CCK8 assay, Hoechst 33342 staining, RT-qPCR, and Western blotting. RESULTS: Compared with WKY rats, SHRs had significantly elevated systolic blood pressure, diastolic blood pressure and mean arterial pressure with significantly increased neuronal apoptosis in the cerebral cortex, reduced expressions of NeuN, miR-124 and Bcl-2, and enhanced expressions of STAT3, Bax and cleaved caspase-3 (P<0.05). All these changes in the SHRs were significantly ameliorated by treatment with QDG (P<0.05). In the HT22 cell model, QDG treatment obviously reduced OGD/R-induced cell apoptosis, increased the expressions of miR-124 and Bcl-2, and suppressed the elevation of protein expressions of STAT3, Bax and cleaved caspase-3. CONCLUSIONS QDG inhibits cerebral cortical neuronal apoptosis and thereby attenuates brain damage in SHR rats by modulating the miR-124/STAT3 signaling axis.
Animals ; Rats, Inbred SHR ; MicroRNAs/metabolism* ; STAT3 Transcription Factor/metabolism* ; Signal Transduction/drug effects* ; Drugs, Chinese Herbal/pharmacology* ; Rats ; Apoptosis/drug effects* ; Rats, Inbred WKY ; Male ; Hypertension

Objective Given that psychosocial stress can contribute to a series of diseases,such as inflammatory bowel disease and irritable bowel syndrome,we aimed to establish an experimental chronic restraint mouse intestinal stress injury model as a basis for exploring the pathogenic mechanism of chronic restraint stress-induced gastrointestinal diseases,and for developing preventive and curative measures.Methods Eighteen male SPF-grade BALB/c mice were acclimatized for 7 days and then divided into a control group and a chronic restraint stress group according to body weight,using a randomized numerical table method.The mice were subjected to restraint stress for 3 hours per day for 14 days to establish an intestinal injury model.The model was evaluated by observing body weight,pathological changes in intestinal histomorphology,expression of tight junction proteins,apoptosis of intestinal epithelial cells,and mRNA expression levels of inflammatory cytokines.Results After 14 days of chronic restraint stress,model mice showed weight loss,shortened duodenal villus height,abnormal crypt structure,a decreased villus/crypt ratio,colonic mucosal inflammatory cell infiltration,and irregular crypt structure.Protein immunoblotting,immunohistochemistry,and immunofluorescence staining showed that the expression levels of the duodenal and colonic tight junction proteins Occludin and Claudin-1 were significantly decreased in mice after chronic restraint stress(P＜0.05),while expression levels of the apoptotic protein cleaved-caspase-3 in intestinal epithelial cells were significantly increased(P＜0.05).Regarding the mRNA expression levels of intestinal inflammatory factors and chemokines,chronic restraint stress for 14 days significantly increased the gene expression levels of interleukin(IL)-1β,IL-6,monocyte chemoattractant protein-1(MCP-1),tumor necrosis factor-α,and IL-10 in the duodenum of mice(P＜0.05),and significantly increased the gene expression levels ofIL-1β,IL-6,and MCP-1 in the colon(P＜0.001).Conclusions The use of a behavioral restriction device to restrain mice continuously for 14 days led to abnormal intestinal tissue structure,intestinal barrier dysfunction,and intestinal epithelial cell apoptosis,and triggered an intestinal inflammatory response in the stressed mice,indicating successful establishment of a mouse model of intestinal injury by chronic restraint stress.

Objective By simulating acute hypoxic conditions, an experimental model of intestinal stress injury in plateau mice was established to explore the pathogenic mechanism of acute gastrointestinal diseases in plateau, and to lay foundation for preventive and therapeutic measures.MethodsThirty-six SPF-grade adult male BALB/c mice were randomly divided into four groups: normoxic 24 h, normoxic 72 h, hypoxic 24 h, and hypoxic 72 h, based on body weight using a randomized numerical table method, with nine mice in each group. Mice in the normoxic group were kept in a conventional barrier environment, while those in the hypoxic group were placed in a hypoxic chamber within the barrier environment with oxygen concentration set at 10% to simulate plateau conditions. They were subjected to stress for 24 h and 72 h, respectively, in order to establish a model of intestinal injury induced by acute hypoxia. After modeling, the mice were weighed, anesthetized with 1% pentobarbital sodium, and then euthanized by cervical dislocation. Duodenal and colonic tissues were collected. Histopathological morphology of intestinal tissues was observed after HE staining. Western blotting and immunohistochemistry were used to detect the expression levels of tight junction-related proteins in intestinal tissues. Real-time fluorescence quantitative PCR was performed to measure the expression levels of inflammatory cytokines and chemokines. TUNEL staining was used to assess apoptotic activity of intestinal epithelial cells, thus evaluating intestinal injury-related phenotypes in this model.Results Compared with the normoxic groups, mice in the 24 h and 72 h hypoxia groups showed weight loss, shortened duodenal villi, abnormal crypt structure, and decreased villus/crypt ratio. The colonic mucosa was infiltrated with inflammatory cells and irregular crypt structure. Expression levels of Occludin and zonula occludens-1 (ZO-1) were significantly decreased in duodenal and colonic tissues of mice in the 24 h and 72 h hypoxia groups (P<0.05). The expression of pro-apoptotic protein Bax was significantly up-regulated while expression of anti-apoptotic protein Bcl-2 was significantly down-regulated in duodenal tissues (P<0.05). Apoptotic activity of intestinal epithelial cells was significantly enhanced (P<0.05). In addition, interleukin (IL)-1β, IL-6, monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor-α (TNF-α) mRNA levels were significantly increased in duodenal tissues after 24 and 72 h of hypoxic stress(P<0.05). After 24 h of hypoxic stress, there was no significant change in the expression levels of inflammatory cytokines in colon tissues (P>0.05), but after 72 h, the expression levels of pro-inflammatory factors IL-1β, TNF-α, IL-6, MCP-1, and anti-inflammatory factor IL-10 mRNAs significantly increased in colon tissues of mice (P<0.05).Conclusion The usage of a hypoxia chamber to simulate an acute hypoxic environment in plateau can lead to abnormal intestinal tissue structure, intestinal barrier dysfunction, and induce intestinal epithelial cell apoptosis, triggering an intestinal inflammatory response in stress mice. These findings indicate the successful construction of a mouse model for an acute hypoxic stress-induced intestinal injury.

The intestine is the largest immune and metabolic site in the body and is thus important for animal health.The integrity of the mucosal barrier and function are fundamental factors protecting the health of the intestine.Stress has been reported to have profound effects on the gastrointestinal tract,including altering gut permeability,the intestinal barrier,and homeostasis.Tryptophan is a functional essential amino acid that alters the gut microbiota and regulates intestine structural and functional change,thus contributing to host physiology and metabolism.Changes in tryptophan metabolism and its metabolites in brain and intestinal tissues during stress suggest that tryptophan may play an important role in the stress response.We therefore review the literature on the mechanisms underlying stress-related diseases and the role of tryptophan metabolism in the regulation of gut homeostasis,with particular focus on functional bowel disorders and their relationship to stress,to provide a theoretical foundation for targeting tryptophan in stress-related intestine diseases.

Objective Through the research and analysis of guangdong medical college affiliated hospital orthopaedic hospitalized patients with a diagnosis of osteoporosis in Zhanjiang,this paper provide theoretical basis for the prevention of osteoporosis frac-ture.Methods The elderly aged over 40 years old,living in this area for a long time.Data was collected from August 2012 to Feb-ruary 2014,hospitalized patients in guangdong medical college affiliated hospital were diagnosed with osteoporosis.Contents include general situation survey,medical examination,venous blood tests and bone mineral density testing.Results Fracture group average age is older than the non fracture group;the fracture group lumbar spine bone mineral density(LSBMD)and femoral neck bone min-eral density(FNBMD)T value and Z value and serum calcium group is greater than the fracture and the differences were statistically significant(P <0.05).Fracture group in gender divided into two groups for comparison,in which women older than men,and the difference was statistically significant(P <0.05),male LSBMD T and Z values and FNBMD T value is greater than the female and the difference was statistically significant(P <0.05).According to the 10 year age group,Each age group compared with the frac-ture number and non fracture number,in the age group of 70-80 fracture number were the most;All age groups in LSBMD,FNB-MD,serum calcium(Ca)and VitD compared,non fracture group is most higher than that of fracture group.The influence factors of the fractures for non conditional Logistic regression analysis,age,LSBMD,FNBMD T value increased were risk factors for fracture, VitD,FNBMD,LSBMD T value increased were protective factors of fracture.Conclusion Need as soon as possible to prevent osteo-porosis,especially before the age of 40,try to improve the peak bone density,to prevent the occurrence of osteoporosis in the future.

Objective To analyze the clinical features of 442 cases of hand-foot and mouth disease in children. Methods A total of 442 cases of hospitalized patients with HFMD in our hospital from January to October 2013 were retrospectively analyzed, according to the patient's age they were divided into group Ⅰ (317 cases), aged 2 months to 3 years old, and groupⅡ (125 cases), aged 3 to 9 years old. General information, laboratory tests, clinical manifestations of different ages were compared. Results Group Ⅰ set the number of leukocytes in children, respiratory rate, EV71-IgM positive rate and CoxA16-IgM were significantly higher than that in group Ⅱ, children of different ages were significant differences (P <0.05), group Ⅰ in fever, diarrhea proportion of patients were higher than in group Ⅱ, children of different ages were significant differences(P<0.05). Conclusion EV71, CoxA16 infection is more common in HFMD children, when children have a fever, symptoms of oral herpes, diarrhea they should treat with active treatment, should pay attention to the prevention of HFMD in children less than 3 years old.

OBJECTIVE: To investigate the effects of Liriope platyphylla total saponin (LPTS) on learning, memory, neuromediators and metabolites in aging mice induced by D-galactose. METHODS: Ninety Kunming mice were randomly divided into nine groups: normal saline (NS)-treated group, untreated group, high- (100 mg/kg), medium- (50 mg/kg) and low-dose (10 mg/kg) LPTS-treated groups, Shuxuening-treated group, jiaogulanosidi-treated group, flunarizine-treated group and vitamin E-treated group. The Kunming mice in the NS-treated group were administered with NS by intraperitoneal injection, while the aging mice in the other eight groups were administered with D-galactose by intraperitoneal injection. At the same time, the aging mice in different groups were fed with corresponding drugs for 42 days, and the aging items of the mice in different groups were measured, respectively. RESULTS: LPTS could improve the memory of aging mice induced by D-galactose, promote its body weight, and increase the thymus and spleen indexes of the aging mice. LPTS could decrease the levels of MDA and lipofuscin, inhibit MAO activity and increase SOD activity and GSH-Px level. CONCLUSION: LPTS may improve the ability of learning and memory and delay aging.

To study the chemical constituents of Fructus Xanthii and to determine the contents of total phenolic acids (TPA) in fruits of Xanthium from different populations for evaluating the quality of them.

OBJECTIVE: To investigate the prevention effect of aqueous extract of Epimedii sagittatum (ESE) on ovariectomy-induced (OVX) bone loss in rats. METHODS: Rats were divided into sham-operated and OVX groups. The OVX rats were divided into four groups treated with distilled water, 17beta-estradiol (1 mg/kg, ig) and ESE (0.5 and 1 g/kg, ig) for 11 weeks. Serum calcium, phosphorus, estradiol, bone gla protein concentrations and serum alkaline phosphatase activity were measured. Bone density was assayed by dual-energy X-ray absorptiometry. The undecalcified longitudinal proximal tibial metaphysical sections were cut and stained for the bone histomorphometric analysis. RESULTS: In OVX rats, alkaline phosphatase activity in serum was markedly increased by ESE treatment, which had no obvious influence on the body weight. Meanwhile, atrophy of uterus and descent of bone mineral density were suppressed by ESE treatment. In addition, ESE completely corrected the decreased concentrations of calcium and E2 in serum observed in OVX rats. Histological results also showed ESE prevented the increases in trabecular separation (Tb.Sp) in OVX rats whereas it did not alter trabecular thickness (Tb.Th) and trabecular number (Tb.N) in OVX rats. Moreover, ESE had remarkable effect on bone formation rate with bone volume as referent (BFR/BV) and bone formation rate with bone surface as referent (BFR/BS). CONCLUSION: The findings assessed on the basis of biochemical test, bone mineral density and histomorphometric parameters show that aqueous extract of Epimedii sagittatum has a definite antiosteoporotic effect and can prevent the OVX-induced bone loss in rats.

Objective To investigate the effects of seed sources and storage conditions on the seed germination rate of Valeriana officinalis. Methods The seeds of V. officinalis under different storage conditions were used as materials for germination test, and the germination rate was calculated and compared according to the results. Results The seed germination rate of valerians is varied with different sources. The seed germination rate of V. officinalis is higher than that of V. officinalis var. latifolia, and the seed germination rate of cultivated valeriana is much higher than that of the wild plant. The storage periods, storage temperature, and germination conditions also affect the germination rate. Conclusion To maintain the seed germination rate, the seed of V. officinalis should be stored in conditions with ventilation and at suitable low temperature. Lower temperature helps to prolong the seed life with relatively high germination rate. Valeriana seed should also be propagated at available temperature conditions in proper seasons.