Objective  To study the nerve repair effect of olanzapine on schizophrenia model rats through its effect on cyclic AMP response element binding protein（CREB）/brain-derived neurotrophic factor（BDNF）/receptor tyrosine kinase receptors B（TrkB）pathway.   Methods  Total 60 rats were divided into control group, model group, olanzapine low, middle and high dose group. The rats in the model group, olanzapine low, middle and high dose groups were injected intraperitoneally with MK-801［0.2 mg/(kg ·d)］, while the control injected with the same amount of normal saline. The low, middle and high dose olanzapine groups were perfused with olanzapine solution of 0.5 mg/(kg ·d),1.0 mg/(kg ·d) and 1.5mg/(kg ·d) respectively. The behavior of rats was scored according to ataxia and stereotyped behavior standards, cognitive function and learning ability were evaluated by Morris water maze test, serum tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels were detected by ELISA method, hippocampal histopathology was observed under microscope, and apoptosis and expression of CREB/BDNF/TrkB pathway related proteins in hippocampus were detected.    Results  Compared with the control group, the ataxia, the score of stereotyped behavior, the expression of TNF-α, IL-6 and the rate of apoptosis in the model group increased significantly (P<0.01). Compared with the control group, the number of crossing the platform, the time of staying in the target quadrant and the relative expression of CREB, p-CREB, p-TrkB, TrkB and BDNF protein in the model group decreased significantly (P<0.01), and those in the low and middle dose olanzapine groups decreased significantly (P<0.05). Compared with the model group, the times of crossing the platform and the stay time in the target quadrant increased significantly in the low and middle dose olanzapine groups (P<0.05). In the model group and the low dose olanzapine group, the hippocampal cells were swollen obviously, the nucleus was broken and divided, pyknosis, and the tissue arrangement was disorderly, while the phenomenon of fragmentation and nuclear pyknosis was rarely seen in the middle and high dose olanzapine groups.   Conclusion  The nerve repair mechanism of olanzapine on schizophrenic model rats is related to improving cognitive impairment, protecting hippocampal neurons and activating the expression of CREB/BDNF/TrkB signal pathway in rats.

Objective  To investigate the structural distribution features and mechanism of elastic fibers and collagen fibers in ventricular interstitium of aged rats.  Methods Five young SD rats (24 weeks) and five old SD rats (104 weeks) were used，and their cardiac function was examined by echocardiography. Modified Weigert elastic fiber staining, immunohistochemistry, immunofluorescence and Western blotting techniques were used to detect the expression changes of type I and Ⅲ collagen fibers and their proteins, elastic fibers and their proteins, matrix metalloproteinase 2 (MMP-2), matrix metalloproteinase 9 (MMP-9) and tissue inhibitor of metalloproteinase 2 (TIMP-2), respectively.    Results The type I and type Ⅲ collagen in the ventricular interstitium of aged rats was very sufficient and wrapped around the cardiomyocytes. Compared with the young rats, the content of collagen protein in the ventricular interstitium of the aged rats significantly increased (P<0.05). Elastic fibers in the ventricular interstitium of the aged rats were and widely distributed. Compared with the young rats, the number of elastic fibers and the level of elastin in the ventricular interstitium of the aged rats significantly decreased (P<0.05), and the expression levels of MMP-2 and MMP-9 in ventricular muscle of aged rats increased, and they were correlated with the level of elastin. The level of TIMP-2 in ventricular muscle of aged rats decreased with age.   Conclusion The number of collagen fibers and elastic fibers in ventricular interstitium of aged rats is fluctuated with each other. With the increase of age, the contents of TIMP-2 and elastic fibers in the ventricular interstitium gradually decreased, and the ratio of collagen fibers to elastic fibers is out of balance.

Objective To improve the fixation method  of the transmission electron microscope for better morphological preservation of mitochondria and lipid droplets in mouse brown adipose tissue.   Methods The fixation method  for mouse brown adipose tissue was optimized, mainly including an increased concentration of paraformaldehyde from 2% to 4% in the pre-fixative, employment of transcardial perfusion followed by immersion fixation in pre-fixation, and using imidazole-buffered osmium tetroxide as the post-fixative. The ultrastructures of brown adipocytes prepared by the improved method  were observed and compared with those of a known standard protocol (3 mice in each group). The improved method  was further validated in the quantitative analysis of mitochondrial cristae density and lipid droplets.   Results The mitochondrial cristae and membrane structure of other organelles of brown adipocytes were better preserved using the optimized method  compared with those of the standard method. Lipid droplets were presented as round structures with high electron density instead of vacuolated appearances. Using this method, we observed that the density of mitochondrial cristae and the content of lipid droplets increased in brown adipocytes after cold adaptation.   Conclusion The optimized method can better preserve the ultrastructure of organelles in brown adipocytes, especially mitochondria and lipid droplets, and may be applicable for studying the ultrastructures remodeling of brown adipose tissue under different physiological or pathological conditions.

Objective To measure and compare the lateral posterior tibial slope (LPTS), medial posterior tibial slope (MPTS) and tibial torsion angle (TTA) between the patients of recurrent patellar dislocation and the heathy people, and to analyze the correlation between LPTS, MPTS and TTA and the risk factors of recurrent patellar dislocation.   Methods  A total of 33 patients (44 knees) with recurrent patellar dislocation in our hospital from July 2019 to June 2021 were selected and listed as the study group. Twenty-three subjects (46 knees) who were suspected iliac vascular and lower limb vascular diseases during the same period were selected and listed as the control group. All the enrolled researchers had full-length CT scans date of the lower limbs. Three-dimensional models were reconstructed using Mimics 21.0 software and then imported into 3-matic software. The LPTS, MPTS and TTA were measured and compared between the two groups.      Results In the study group, the LPTS, MPTS and TTA were （7.69±1.42）°,（10.06±1.71）°,（36.42±8.13）°, respectively, while the control group, the LPTS, MPTS and TTA were（8.42±1.65）°, （10.44±0.86）°, (25.77±3.90)°, respectively. There were no significant differences in the LPTS, MPTS and TTA between different genders and sides both in the study group and the control group (P>0.05). Compared with the control group, the LPTS in the study group was smaller, and the difference was statistically significant (P<0.05). There was no statistically significant difference between the study group and the control group in the MPTS (P>0.05). Compared with the control group, the TTA in the study group was higher, and the difference was statistically significant (P<0.05). Compared with the control group, the LPTS and MPTS in the study group were significant asymmetry, and the difference was statistically significant (P<0.05).  Conclusion The lateral posterior tibial slope of patients with recurrent patellar dislocation is significantly smaller than that in the healthy people, while there is no significant difference in the medial posterior tibial slope; The tibial torsion angle of patients with recurrent patellar dislocation is significantly larger than in the healthy people; The lateral posterior tibial slope and tibial torsion angle have certain correlation with recurrent patellar dislocation, which can conduct the diagnosis of recurrent patellar dislocation.

Objective  To study the role of complement C3a receptor (C3aR) in cognitive impairment in rats with sepsis induced by cecal ligation and puncture (CLP), and to explore the possible mechanism.   Methods  Totally  132 rats were randomly divided into sham operation group (sham group) and sepsis group (CLP group). The initial number of each group was 66 animals, and 22 animals were set at each time point. The SD rat CLP animal model was constructed, and serum and brain (hippocampus and prefrontal cortex) samples were collected at day 1, day 15 and day 30 after operation. The levels of tumor necrosis factor-α(TNF-α), interleukin-1β (IL-1β) and IL-6 in the samples were determined by ELISA. Western blotting detected Tau protein (Tau), phosphorylated Tau（p-Tau）and C3aR expression in brain samples. Totally 66 rats were randomly divided into 3 groups, sham operation group, CLP group and C3aR antagonist(C3aRa) intervention group. On 15th, 17th, and 19th days after CLP, C3aRa intervened in rats, and they received inhibition avoidance test and object recognition test 30 days after CLP. The expressions of C3aR, lonized calcium binding adapter molecule 1(Iba1), GFAP and p-Tau in the hippocampus were detected by immunofluorescence.   Results  Compared with the sham group, the serum and brain tissue (TNFα, IL-1β and IL-6) of rats in the CLP group first increased and then decreased within 30 days after CLP. In the hippocampus and prefrontal cortex of CLP group, Tau phosphorylation was significantly enhanced at day 30 and day 1 and 15 after surgery, respectively (P<0.05). Compared with the sham group, C3aR protein levels in hippocampus and prefrontal cortex of rats in CLP group increased significantly at day 15 and 30 after operation (P<0.05). Compared with the CLP group, the endogenous C3aR content decreased significantly after C3aRa intervention (P<0.05), and Iba1, GFAP and p-Tau immunostaining were significantly inhibited (P<0.05). The C3aRa intervention in CLP rats reversed the cognitive impairment.   Conclusion  C3aR plays an important role in the development of biochemical and behavioral changes commonly associated with the onset of sepsis-induced neurodegenerative processes. C3aRa can be injected into the hippocampus to counteract the neurodegenerative process induced by sepsis.

Objective To explore the effect of interleukin (IL)-6 on nucleated erythrocytes in lipopolysaccharide (LPS)-induced preeclampsia rats.  Methods ELISA and immunohistochemistry were used to detect the IL-6 in peripheral blood and placenta of preeclampsia and normal pregnancy; Flow cytometry and immunofluorescence were used to detect the maternal nucleated erythrocytes. Pregnant SD rats were randomly divided into 3 groups: the control, LPS and LPS +anti-IL-6 group; IL-6, the proportion of nucleated erythrocytes, JAK2/MEK and PI3K/Akt signal-related genes were detected.  Results The IL-6 of preeclampsia was higher than that of normal patients. Compared with the Control group, IL-6, the proportion of nucleated erythrocytes and JAK2, P85, Akt, P65, IL-1B mRNA of LPS group increased, the fetal weight decreased; Compared with the LPS group, IL-6, the proportion of nucleated erythrocytes and JAK2, P85, Akt, P65 and IL-1B mRNA of the LPS+anti-IL-6 group decreased.   Conclusion The up-regulation of IL-6 of preeclampsia patients is accompanied by increased nucleated erythrocytes in peripheral blood. Neutralizing IL-6 in vivo may down-regulate JAK2/PI3K/Akt/NF-κB-signal-mediated IL-1B to protect preeclampsia rats.

Objective  To investigate the relieving effects of knockdown of long non-coding RNA（lncRNA）taurine up-regulated gene 1 (TUG1) on inhibiting nucleotide binding oligomerization domain like receptor protein 1(NLRP1) inflammasome and the progression of Alzheimer’s disease.    Methods  Wild-type (WT group,10 mice) or amyloid precursor protein (APP)/presenilin-1 (PS1) transgenic mice (30 mice) with a genetic background of C57/BL6 aged 9-10 weeks were used in this study. APP/PS1 transgenic mice were randomly divided into model group, model+lncRNA TUG1 short hairpin RNA (shRNA) group and model+shRNA non target（NT）group (n=10). Blood samples, cerebral cortex tissues, primary microglial cells and primary astrocytes were collected from mice 12 weeks of age on day 1 (3-month-old) and 32 weeks of age on day 1 (8-month-old), with 5 mice per group at each time point. Real-time PCR analysis was used to detect the expression levels of lncRNA TUG1 and macrophage migration inhibitory factor (MIF) mRNA in cerebral cortex tissues and primary microglial cells, and C1r and C1s mRNA levels in primary astrocytes of 3-month-old and 8-month-old mice in the above 4 groups, respectively. ELISA was used to determine the MIF in plasma samples of the above 4 groups of mice. Primary microglia and astrocytes from the cerebral cortex of 3-month-old and 8-month-old mice were co-cultured. CCK-8 method  was used to determine the proliferation ability of the above cells. Western blotting was used to determine the expression levels of MIF, pro interleukin-1β(pro-IL-1β), apoptosis associated speck-like protein containing a caspase recrult domain(ASC), Caspase-1 (p20), Caspase-1 (full), NLRP1 and NLRP3 in cerebral cortex tissues of 3-month-old and 8-month-old mice. Immunofluorescent staining was used to determine amyloid beta（Aβ）in cerebral cortex of 8-month-old mice.    Results  At the age of 3-month-old and 8-month-old, compared with the WT group, the relative expression level of lncRNA TUG1 and MIF in cerebral cortex tissues and primary microglia of model group mice was significantly up-regulated, with primary microglial cells and astrocytes proliferation ability enhanced (P<0.05). Compared with the model group, the relative expression level of lncRNA TUG1 and MIF cerebral cortex tissues and primary microglia of model+lncRNA TUG1 shRNA group were significantly down-regulated, with primary microglial cells and astrocytes proliferation ability decreased (P<0.05). Compared with the WT group, MIF factor in the peripheral plasma of model group increased significantly, with pro-IL-1β，ASC，Caspase-1 (p20)，Caspase-1 (full), NLRP1 and NLRP3 expression level up-regulated in the model group mice cerebral cortex tissues, with increased Aβ immunofluorescent indensity (P<0.05). Compared with the model group, MIF factor in the peripheral plasma, and pro-IL-1β，ASC，Caspase-1 (p20)，Caspase-1 (full) and NLRP1 expression in the model+lncRNA TUG1 shRNA group mice cerebral cortex tissues were down-regulated, and Aβ immunofluorescent indensity decreased (P<0.05), while NLRP3 expression level were not changed (P>0.05). There was no significant difference between the model group and the model+shRNA NT group mice of all the above factors (P>0.05).   Conclusion  In APP/PS1 transgenic mice, up-regulation of lncRNA TUG1 and MIF are positively associated with the activation of NLRP1 inflammasome in mice cerebral cortex tissues and primary microglia. Knock-down of lncRNA TUG1 can ameliorate the progression of Alzheimer’s disease.

Objective  To investigate the effect of microRNA (miR)-138 regulation of Wnt signaling pathway on the biological behavior of human glioma cells in vitro.    Methods  Glioma cell lines U-87MG and U251 were selected and randomly divided into blank group, miR-NC group, miR-138 mimics group and miR-138 inhibitor group. Real-time PCR was used to detect the miR-138 expression in each group; MTT, flow cytometry, Transwell assay and scratch assay were used to detect proliferation, apoptosis, invasion and migration ability of each group respectively, and Western blotting was used to detect Wnt pathway related protein expression in each group.   Results  The miR-138 expression level was higher in the miR-138 mimics group compared with the remaining 3 groups, and that in the miR-138 inhibitor group was lower than that in the blank group and the miR-NC group (P<0.05); Compared with the blank group, the cell proliferation rate was lower in the miR-138 mimics group and higher in the miR-138 inhibitor group, and was time-dependent(P<0.05); The apoptosis rate in the miR-138 mimics group was higher than that in the blank group, miR-NC group, and miR-138 inhibitor group, while the apoptosis rate in the miR-138 inhibitor group was lower than that in the rest other groups(P<0.05); The number of cell-invading cells in the miR-138 mimics group was lower than that in the blank group, miR-NC group, and miR-138 inhibitor group, while all miR-138 inhibitor group were higher than the remaining three groups (P<0.05); The cell migration rate of miR-138 mimics group was lower than that of blank group, miR-NC group and miR-138 inhibitor group, while all miR-138 inhibitor group were higher than the remaining three groups (P<0.05); Wnt3a, Wnt1, glycogen synthase kinase 3β(GSK-3β)  and β-catenin protein expression in the miR-138 mimics group was lower than that in the blank group, miR-NC group, and miR-138 inhibitor group; While miR-138 inhibitor groups were higher than the remaining three groups(P<0.05).   Conclusion  MiR-138 overexpression effectively inhibite the proliferation, invasion and migration of glioma cells and promote their apoptosis, probably achieved by pathway inhibition of the Wnt signaling pathway.

Objective  To observe the expression and localization of group Ⅰ metabotropic glutamate receptors (mGluR1/5) in rat superior cervical ganglion (SCG) and the effect of chronic intermittent hypoxia (CIH) on mGluR1/5 protein level.   Methods  Twelve male SD rats were randomly divided into control group（Ctrl）and CIH group（CIH）, 6 rats in each group. After 6 weeks of modeling, the effect of CIH on mGluR1/5 protein level was detected by Western blotting, the expression and distribution of mGluR1/5 in SCG were detected by immunohistochemistry and double-immunofluorescent staining.     Results  mGluR1/5 was expressed in rat SCG. mGluR1 was distributed in neurons and small intensely fluorescent (SIF) cells, but not in satellite glial cells (SGCs), nerve fibers and blood vessels, whereas mGluR5 was mainly distributed in nerve fibers and a little in neurons, but not in SGCs, SIF cells and blood vessels. CIH increased the protein levels of mGluR1/5 (P<0.01) in rat SCG.   Conclusion  Both mGluR1 and mGluR5 are expressed in the rat SCG, but their distribution are different, and the increased protein levels of both may be involved in CIH-induced hypertension.

Objective To analysis risk factor and to construct a line graph prediction model for bone cement leakage after percutaneous transluminal vertebroplasty treatment in patients with osteoporotic spinal compression fractures.   Methods A total of 236 patients with osteoporotic spinal compression fractures who came to our hospital from December 2019 to December 2021 were selected for the study, and they were divided into a leakage group (n=58) and a non-leakage group (n=178) according to whether bone cement leakage occurred after percutaneous transluminal vertebroplasty treatment. The clinical data were collected to analyze the factors associated with bone cement leakage; The work receiver operating characteristic(ROC) curves of the subjects were drawn to analyze the predictive value of each relevant factor on bone cement leakage; The Logistic multiple regression model was used to analyze the risk factors affecting bone cement leakage; The R language software 4.0 “rms” package was used to construct the prediction model of column line diagram.   Results The differences in age, bone density, degree of vertebral compression, vertebral endplate/posterior wall integrity, bone cement viscosity, and bone cement injection volume between patients in the leaky and non-leaky groups were statistically significant (P<0.05). The area under curve(AUCs) for age, bone density, and cement injection volume to predict cement leakage were 0.804, 0.825, and 0.803, respectively; The best cutoff values were 71 years, 0.67 g/cm2, and 4.4 ml, respectively. Age (>71 years), bone density (≤0.67 g/cm2), vertebral compression (severe), vertebral endplate/posterior wall integrity (no), cement viscosity (low viscosity), and bone cement injection volume (>4.4 ml) were independent risk factors for bone cement leakage. The column line graph model predicted a C-index of 0.802 (95% CI , 0.689-0.868) for cement leakage, with a threshold >0.19, and the column line graph model provided a net clinical benefit.  Conclusion Age, bone density, degree of vertebral compression, vertebral endplate/posterior wall integrity, cement viscosity, and cement injection volume are independent risk factors for cement leakage, and the column line graph prediction model constructed with these predictors is of clinical application.

Objective  To investigate the protective effect and mechanism of liraglutide on the paraquat (PQ)-induced Parkinson’s disease (PD) mouse model.      Methods  Totally 24 Kunming mice were randomly divided into control group, PQ group and PQ +liraglutide group, 8 mice in each group. PD model was established by intraperitoneal injection of PQ (10 mg/kg) for 5 consecutive days, and liraglutide (50 nmol/kg) was injected intraperitoneally for 7 consecutive days. The free-standing and locomotor activity of mice were measured by behavioral method. Immunofluorescence was used to observe the number of tyrosine hydroxylase (TH) and ionized calcium binding adaptor molecule 1 (Iba1) immunoreactive cells. Western blotting was used to detect the expression of protein TH, glial fibrillary acidic protein (GFAP), mitofusin-2 (Mfn2) and dynamin-related protein 1 (Drp1).    Results  The numbers of free-standing and locomotor activity numbers decreased significantly (P<0.01, P<0.05) in PQ group compared with the control group, and the number of TH immunoreactive cells and TH protein expression in substantia nigra decreased significantly (P<0.01, P<0.01) compared with the control group, while the number of Iba1 immunoreactive cells and GFAP protein expression increased significantly (P<0.01, P<0.01) compared with the control group; the expression of Drp1 protein in PQ group was significantly higher than that in control group (P<0.05), while the Mfn2 protein expression decreased significantly (P<0.05) compared with the control group. After treatment with liraglutide, the number of TH positive cells in PQ + liraglutide group was significantly lower than that in control group (P<0.05); the numbers of free-standing and locomotor activity increased significantly (P<0.05, P<0.05) in PQ + liraglutide group compared with the PQ group, and the number of TH positive cells and expression of TH protein in PQ + liraglutide group were significantly higher than that in PQ group (P<0.01, P<0.01); while the number of Iba1 positive cells and GFAP protein expression decreased significantly (P<0.01, P<0.05) compared with the PQ group; the Drp1 protein expression decreased significantly (P<0.01) compared with the PQ group, while the expression of Mfn2 protein in PQ + liraglutide group was significantly higher than that in PQ group (P<0.01).   Conclusion  Liraglutide has neuroprotective effect by reducing neuroinflammation in substantia nigra, regulating mitochondrial fusion and fission.

Objective  To observe the potential mechanism of electroacupuncture regulating the erythropoietin-producing hepatocellular receptor B2/erythropoietin-producing hepatocellular receptor-interacting B2/big mitogen-activated protein kinase 1(EphB2/EphrinB2/BMK1) signaling pathway to improve neural damage in vascular dementia rats.   Methods  Eighty SD male adult rats were randomly divided into a sham surgery group, a model group, a non acupoint electroacupuncture group, a nimodipine group, and an electroacupuncture three needle group. The vascular dementia rat model was made by the modified Pulsinelli four vessel occlusion method. After grouping, the rats in each group were subjected to water maze test, HE staining, Nissl staining, and transmission electron microscopy(TEM) to observe the pathological changes in the hippocampal CA1 area, and the expression of EphB2 and BMK1 in the hippocampal CA1 area was detected by immunohistochemistry; Detection of EphB2 and BMK1 protein expression in rat hippocampal CA1 region was detected by Western blotting.    Results  Compared with the model group, the escape latency of vascular dementia rats treated with electroacupuncture and nimodipine decreased (P<0.05), while the number of crossing platforms significantly increased (P<0.05); The result of HE staining, Nissl staining and TEM showed that compared with the model group, the neurons in hippocampal CA1 area of rats in the EA Zhisanzhen group and nimodipine group were arranged orderly, and the morphology and structure of cells and organelle were complete; Immunohistochemical method  and Western blotting showed that the expression of EphB2 and BMK1 in the CA1 region of hippocampus in the model group was significantly lower than that in the sham surgery group (P<0.05); Compared with the model group, the expression of EphB2 and BMK1 in the hippocampal CA1 region of rats in the electroacupuncture Zhisanzhen group significantly increased (P<0.05), while the expression of EphB2 and BMK1 in the hippocampal CA1 region of rats in the non acupoint electroacupuncture group was not statistically significant (P>0.05). Compared with the nimodipine group, the expression of EphB2 and BMK1 in the hippocampal CA1 region of rats in the electroacupuncture Zhisanzhen group significantly increased (P<0.05).   Conclusion  Electroacupuncture may improve the damage of hippocampal neurons in vascular dementia rats by increasing the expression of EphB2 and BMK1 in the CA1 region of the hippocampus, thereby improving the learning and memory of vascular dementia rats.

 Objective To analyse the analgesic effect and possible mechanism of panax notoginseng saponin (PNS) on mouse models of chronic inflammatory pain caused by complete Freund’s adjuvant (CFA).   Methods A total of 48 male C57BL/6J mice were divided randomly into four groups: normal saline control group (Ctrl), CFA group (CFA), CFA + PNS group (CFA+PNS), CFA + dexamethasone (DEX) group (CFA+DEX). Von Frey filaments were used to detect mechanical pain in mice. Immunohistochemistry was used to detect the number and morphological changes of glial fibrillary acidic protein (GFAP) positive astrocytes. Western blotting was used to detect the expressions of GFAP, nucleotide-binding and oligomerization domain(NOD)-like receptor thermal protein domain associated protein 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC), Caspase-1, interleukin (IL)-1β, and IL-18 in mice’s spinal cord segments in each group.   Results Compared with the Ctrl group, mice in the CFA group showed a significant decrease in mechanical pain thresholds at day 1, day 3, day 5, day 7, and day 14. Additionally, there was a significant decrease in NLRP3, ASC, Caspase-1, IL-1β and IL-18 in the spinal cord of the mice. PNS intervention could relieve mechanical pain and down-regulate the expressions of NLRP3, ASC, Caspase-1, IL-1β and IL-18 in the spinal cord of mice, with no significant difference compared with the CFA+DEX group. CFA group mice had significantly more GFAP positive cells in their posterior horns than Ctrl group mice, as measured by immunohistochemistry; PNS intervention decreased the number of GFAP positive cells in the posterior horn of the spinal cord in model mice；DEX had no effect on the number of GFAP positive cells in the dorsal horn of spinal cord. According to Western blotting results, GFAP expression in the spinal cord of the CFA group was significantly more than that of the Ctrl group; PNS intervention significantly reduced GFAP expression in the spinal cord of CFA group mice；DEX had no effect on the expression of GFAP in the posterior horn of spinal cord.   Conclusion PNS has a good alleviating effect on inflammatory pain, and its mechanism may be related to inhibition of astrocyte activation and NLRP3 inflammasome activation. 

Objective To analyze the nutritional level, obesity status and the prevalence of hypertension in Blang, Deang and Va ethnic groups in Yunnan, to explore the relationship among nutritional physical index, obesity indicators and blood pressure, and use the cutoff value of related indicators to warn hypertension.  Methods This paper was based on a statistical analysis of the 7 nutritional physical indexes, 5 types of obesity status and hypertension status of 766 Blang, 570 Deang and 565 Va.   Results  We found that the nutritional physique index of many items (4 items for men and 4 items for women) of Blang was significantly higher than that of Deang and Va (P<0.05), the Erismann’s index and Pelidisi’s index of Deang female were significantly higher than those of Blang female and Va female (P<0.05). The differences in the obesity rates determined by the three obesity determination indexes of waist circumference(WC), waist-to-hip ratio(WHR) and percent of body fat(PBF)were statistically significant among the three ethnic groups (P<0.05), and the obesity rates determined by the three indexes of body mass index (BMI), body adiposity index (BAI) and PBF were all the highest in the Blang, and the central obesity rates determined by the two indexes of WC and WHR were all the highest in Va. The rank of the prevalence of hypertension was Va > Blang > Deang and the difference was statistically significant (P<0.05). Conclusion Pelidisi’s index, WHR, and PBF all have good early warning effects on hypertension in all three ethnic groups.