BACKGROUND: Panax notoginseng is an effective medicine for curing gastric mucosal ulcer. There are many clinical reports that Panax notoginseng protects gastric mucosa.OBJECTIVE: To investigate the protective mechanism of Panax notoginseng on the gastric mucosal injury induced by water immersion restraint stress in rats.DESIGN: A randomized controlled animal trial.SETTING: School of Basic Medical Sciences, Daqing Branch of Harbin Medical University.MATERIALS: The study was conducted in the laboratory of Department of Pathophysiology of Harbin Medical University from September 2004 to October 2005. Forty-eight Wistar rats were used, either male or female, weighing 180-230 g.METHODS: The 48 Wistar rats were randomly divided into six groups with 8 rats in each group: normal control group, stress model group, cimetidine treatment group, Panax notoginseng of low, middle and high-dose groups (4, 8, 12 mg/time). In the cimetidine treatment group, cimetidine tablets were grinded into powders, then mixed with distilled water to prepare into suspension (1 tablet:10 mL), which was perfused intragastrically (5 mL), 3 times a day; In the Panax notoginseng groups, the powders in Panax notoginseng capsules were mixed with distilled water to prepare into suspension of corresponding concentrations (0.8, 1.6, 2.4 g/L), then administrated the same as those in the cimetidine treatment group. Stress models in rats were established by means of water immersion restraint stress. The gross and pathohistological changes of gastric mucosa were observed, and the activity of superoxide oxidase (SOD) and contents of malondialdehyde (MDA) and nitric oxide (NO) were determined.MAIN OUTCOME MEASURES:①Gross and pathohistological changes of gastric mucosa;②Changes of MDA and NO contents and SOD activity in the homogenate of gastric mucosa.RESULTS: All the 48 rats were involved in the analysis of results. The gastric mucosal hemorrhage and erosion in the cimetidine treatment group were reduced obviously as compared with those in the stress model group, SOD activity was obviously decreased [(12.61±0.87), (1.03±0.60) mkat/g], whereas the NO content was a little higher [(5.76±1.35), (0.97±0.58) nmol/g]. The MDA content was obviously higher in the stress model group than in the normal control group [(3.10±1.13), (0.09±0.02) μmol/g, P＜0.01]. There were no obvious differences between the Panax notoginseng groups and the cimetidine treatment group except that the NO contents were decreased in the in Panax notoginseng groups.CONCLUSION: Gastric mucosal injury induced by water immersion restraint stress can be significantly protected by Panax notoginseng, which is not dose-dependent. The protective mechanism may be associated with that Panax notoginseng can eliminate the product of oxygen-derived free radicals, and it is not totally the same as that of cimetidine

Objective:To investigate the relationship between serum vascular endothelial growth factor (VEGF), peripheral blood microRNA-126 (miR-126) and the number and distribution of cerebral microbleeds (CMBs).Methods:Consecutive patients with non-acute ischemic cerebrovascular disease admitted to the Department of Neurology, the First Affiliated Hospital of Baotou Medical College from June 2019 to June 2020 were enrolled. The clinical data were collected, 3.0 T MRI examination was performed, and susceptibility-weighted imaging was used to detect CMBs. The serum VEGF concentration was detected by enzyme-linked immunosorbent assay, and miR-126 was detected by fluorescence quantitative polymerase chain reaction. Multivariate logistic regression analysis was used to determine the independent influencing factors of CMBs. Multiple linear regression analysis was used to determine the correlation between serum VEGF concentration, miR-126 in peripheral blood and the number of CBMs. Receiver operating characteristic (ROC) curve was used to evaluate the predictive value of serum VEGF concentration and relative expression of miR-126 in peripheral blood for CMBs. Results:A total of 193 patients with non-acute ischemic cerebrovascular disease were enrolled, including 110 patients (57.0%) in the non-CMBs group, 20 (10.4%) in the strictly lobar CMBs group and 63 patients (32.6%) in non-strictly lobar CMBs group. The comparison among the three groups showed that age might be a risk factor for strictly lobar CMBs, while higher VEGF, higher cystatin C level, lower relative expression of miR-126 in peripheral blood, hypertension and previous stroke or transient ischemic attack might be the risk factors for non-strictly lobar CMBs. Multivariate logistic regression analysis showed that higher serum VEGF concentration was an independent risk factor for non-strictly lobar CMBs (odds ratio 1.186, 95% confidence interval 1.035-1.358; P=0.014), while the higher relative expression of miR-126 was an independent protective factor for non-strictly lobar CMBs (odds ratio 0.154, 95% confidence interval 0-0.269; P=0.026). Multiple linear regression analysis showed that higher serum VEGF concentration ( r=0.848, P<0.001) and the lower relative expression of miR-126 ( r=-0.043, P=0.035) significantly increased the number of CMBs. ROC curve analysis showed that the area under the curve of serum VEGF for predicting non-strictly lobar CMBs was 0.803 (95% confidence interval 0.741-0.865), the optimal cut-off value was 120.55 ng/L, the sensitivity was 70.7%, and the specificity was 75.5%. Conclusions:In patients with non-acute ischemic cerebrovascular disease, there is a significant correlation between serum VEGF concentration and the relative expression of miR-126 in peripheral blood and the number and distribution of CMBs. Serum VEGF can be used as a biomarker for predicting the presence of non-strictly lobar CMBs.

Objective: To observe the effect of Tuina (Chinese therapeutic massage) on creatine kinase (CK), mitochondrial Ca2+ concentration, and ultrastructure of skeletal muscle in delayed onset muscle soreness (DOMS) model rats.Methods: A total of 130 healthy male Sprague-Dawley rats were randomly divided into a blank group, an exercise control group, a pre-exercise Tuina group, and a post-exercise Tuina group. According to the time points for sample collection, the exercise control group was divided into a 0 h exercise control group, a 24 h exercise control group, a 48 h exercise control group, and a 72 h exercise control group; the pre-exercise Tuina group was further divided into a 0 h pre-exercise Tuina group, a 24 h pre-exercise Tuina group, a 48 h pre-exercise Tuina group, and a 72 h pre-exercise Tuina group; and the post-exercise Tuina group was divided into a 0 h post-exercise Tuina group, a 24 h post-exercise Tuina group, a 48 h post-exercise Tuina group, and a 72 h post-exercise Tuina group. Rats in all groups except for the blank group received DOMS modeling. Professionals performed Nie-Pinching manipulation and finger Nian-Twisting manipulation on the lower limbs of the rats. The samples were collected at 0 h, 24 h, 48 h, or 72 h after exhaustive exercise for each pre-exercise Tuina group. The samples were collected at 0 h, 24 h, 48 h, or 72 h after Tuina for each post-exercise Tuina group. The changes in serum CK, skeletal muscle mitochondrial Ca2+ concentration, and Ca2+-adenosine triphosphatase (ATPase) were determined. The ultrastructure changes of skeletal muscles in each group were observed by a transmission electron microscope. Results: The electron microscope showed that compared with the exercise control group, the skeletal muscle structures of the pre-exercise Tuina group and the post-exercise Tuina group were significantly improved, and the overall performance of skeletal muscle in the pre-exercise Tuina group was more similar to that of the blank group. The level of serum CK in the pre-exercise Tuina group and the post-exercise Tuina group was significantly lower than that in the exercise control group (P<0.01). The Ca2+ concentration of skeletal muscle in the 24 h, 48 h, and 72 h pre-exercise Tuina groups was lower than that in the post-exercise Tuina group at the same time point (P<0.01). The Ca2+-ATPase concentration of skeletal muscle in the 24 h and 72 h pre-exercise Tuina groups was lower than that in the post-exercise Tuina group at the same time point (P<0.05).Conclusion: Tuina effectively prevents muscle damage caused by heavy exercise and long-term exercise, which may be related to the increase of skeletal muscle Ca2+-ATPase activity and mitochondrial Ca2+ transport.

Objective To investigate the application value of combination of thinprep cytologic test (TCT),human papilloma virus (HPV),c-MYC and human chromosome telomerase gene (hTERC) genes to screen cervical cancer.Methods A total of 230 cases of the study objects was detected with TCT and HP,respectively.Amplification of c-MYC and hTERC genes was tested with fluorescence in situ hybridization (FISH) method.The histopathological results were the gold standard,and the sensitivity,specificity and accuracy of cervical intraepithelial neoplasia (CIN) Ⅱ / Ⅲ and squamous cell carcinoma (SCC) were compared with the four combined detection.Results Of 230 screened patients,there were 124 cases of TCT positive,155 cases of HPV positive,c-MYC gene amplified in 118 cases,and hTERC gene amplified in 128 cases.When TCT,HPV,c-MYC,and hTERC were used alone,the highest sensitivity was HPV (84.5％),the highest specificity was c-MYC (97.6％),and the highest accuracy was hTERC (85.2％).When the three indexes were used in coordination with each other,the sensitivity and accuracy of TCT + HPV + hTERC were the highest (98.6％ and 90.9％),and the specificity of TCT + c-MYC + hTERC was the highest (79.3％).When the four indexes were used together,the sensitivity was 98.6％,the specificity was 72.0％,and the accuracy was 89.1％.Conclusions Combined examination can improve the sensitivity and accuracy of screening cervical lesions,and the three combination of TCT + HPV + hTERC had the best effect,and c-MYC gene detection had the highest specificity.

Pentaxin 3 (PTX3), as a multifunctional glycoprotein, plays an important role in regulating inflammatory response, promoting tissue repair, inducing ectopic calcification and maintaining bone homeostasis. The effect of PTX3 on bone mineral density (BMD) may be affected by many factors. In PTX3 knockout mice and osteoporosis (OP) patients, the deletion of PTX3 will lead to decrease of BMD. In Korean community "Dong-gu study", it was found that plasma PTX3 was negatively correlated with BMD of femoral neck in male elderly patients. In terms of bone related cells, PTX3 plays an important role in maintaining the phenotype and function of osteoblasts (OB) in OP state;for osteoclast (OC), PTX3 in inflammatory state could stimulate nuclear factor κ receptor activator of nuclear factor-κB ligand (RANKL) production and its combination with TNF-stimulated gene 6(TSG-6) could improve activity of osteoclasts and promote bone resorption;for mesenchymal stem cells (MSCs), PTX3 could promote osteogenic differentiation of MSCs through PI3K/Akt signaling pathway. In recent years, the role of PTX3 as a new bone metabolism regulator in OP and fracture healing has been gradually concerned by scholars. In OP patients, PTX3 regulates bone mass mainly by promoting bone regeneration. In the process of fracture healing, PTX3 promotes fracture healing by coordinating bone regeneration and bone resorption to maintain bone homeostasis. In view of the above biological characteristics, PTX3 is expected to become a new target for the diagnosis and treatment of OP and other age-related bone diseases and fracture healing.
Animals ; Male ; Mice ; Bone Resorption/metabolism* ; Cell Differentiation ; Fracture Healing/genetics* ; Osteoblasts ; Osteoclasts ; Osteogenesis ; Osteoporosis/genetics* ; Phosphatidylinositol 3-Kinases/pharmacology*