Transient receptor potential vanilloid 1(TRPV1) pathway is a non selective cation pathway, which can be activated by various stimulators such as capsaicin and high temperature, and participate in many physiological and pathological processes. As is confirmed by the latest research that the TRPV1 pathway is a core factor of mechanism of nerve immune regulation network, which plays an important role in nasal mucosa in allergic rhinitis. This article is a brief review about the research progress of TRPV1 regulating and controling neuropeptides by neural immunoregulation network which could influence the symptoms of nasal mucosa. It is expected to provide theoretical basis for clinical treatment of allergic rhinitis.

Macrophages have the great plasticity in various tissues in vivo, which play important roles in the development and homeostasis. In response to certain inductors, macrophages can change their phenotype and result in polarization. Polarized macrophages can react to the immune response and participate in tissue repair and remodeling, which have the significant clinic application value. In this review, the classification, regulation mechanism and reprogramming of polarization are addressed, which may provide a theory basis for research of macrophage polarization.

 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 assess the differences in behavior and molecular mechanism of C57BL/6 mice subjected to repeated corticosterone injection (CORT) or chronic unpredictable mild stress (CUMS), and to provide a theoretical reference for antidepressants screening and evaluation. Methods Thirty male C57BL/6 mice were divided into control group, CORT group and CUMS group. During the 3 week stress period, body weights of mice were measured every 3 days. After stress exposure, the open-field test, force swimming test and tail-suspension test were used to evaluate the behavioral changes, with serum corticosterone measured by ELISA. Histological studies were carried out the hippocampal neuron damage with Nissl staining, while the expressions of brain CRH, BDNF, p-CREB and p-ERK protein or gene transcripts were analyzed by Western blotting or PCR. Results Compared with the control group, the number of grooming was significantly decreased in the CORT group, with no significant changes in frequency of crossing and rearing. In the CUMS group, the numbers of rearing and crossing were significantly decreased, while the frequency of grooming was not changed. In the force swimming and tail suspension tests, the time of immobility was significantly increased in both CORT and CUMS groups compared with the control group. Serum corticosterone levels were significantly higher in CORT and CUMS groups than control group. Comparing between the two model and the control groups, there was no significant difference in the thymus index, while the spleen index in the CORT group was significantly decreased. The density of CA1, CA3 and dentate gyrus regions Nissl stained neurons reduced in both CUMS and CORT group, especially in CORT group. Through PCR detection, levels of brain CRH mRNA in both CORT and CUMS group were significantly higher than the control group. Levels of BDNF, p-CREB and p-ERK protein were decreased in the CORT and CUMS groups relative to control, whereas CRH protein levels were higher in the former two groups. Conclusion Both the CORT and CUMS models present depression behaviors, which appears to reflect dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis. There is no significant difference between CORT and CUMS models in behavior alteration, hippocampal formation and protein expression of BDNF-p-CREB and ERK signaling pathway. In conclusion, the CORT model could be a useful model of depression and might be applied for mechanism research and antidepressant screening. The CORT model has an advantage of simple operation and shorter modeling cycle over the CUMS model.

Objective To observe the effect of different fixative solutions on cancer cell morphology and membrane permeability. Methods Human pancreatic acinar epithelial carcinona(HPAC) cells of human pancreatic cancer and HeLa cells of human cervical cancer were fixed with 4 fixation solutions: freshly prepared 0.25% paraformaldehyde solution; Freshly prepared 4% paraformaldehyde solution; 75% ethanol solution; 90% ethanol solution. The fixation time is 30 minutes. PBS solution and complete medium were used as the controls. Cell morphology of each group was observed under optical microscope. Changes in cell membrane permeability were observed by fluorescence staining with 7-aminoactinomycin (7-AAD), which is not cell membrane permeable in intact cells but permeable in damaged cells. Hoechst33342 was used for staining both intact and damaged cells. Results The cells in the complete medium group were similar to unfixed cells in morphology, and the fluorescence staining of 7-AAD was the weakest. The cells in the complete medium group have typical cell morphology and low 7-AAD permeability. The 0.25% paraformaldehyde solution group had similar cell morphology to the complete medium group, and the 7-AAD fluorescence staining was weak. The morphology of cells in the 4% paraformaldehyde solution group was typical, but the fluorescence staining of 7-AAD was strong. The cells in the 90% ethanol solution group showed swelling, with a larger volume than the unfixed cells and a stronger fluorescence staining of 7-AAD. The cell swelling in 75% ethanol solution group was not as obvious as that in 90% ethanol solution group, and the fluorescence staining of 7-AAD was strong. The cells in PBS group were round, and the fluorescence staining of 7-AAD was strong. Conclusion 0.25% paraformaldehyde solution can not only fix tumor cells, but also maintain the integrity of cell membrane.

Objective To investigate the mechanisms of pain hypersensitivity to lowdose capsaicin in a mouse model of chronic compression of dorsal root ganglion (CCD). Methods Chronic compression of L4 DRG was performed in mice by inserting an L-shaped stainless steel rod into the L4 intervertebral foramina. Different doses of capsaicin（0.01, 0.1, 1 g/L）1 μl were injected into the skin on the calf area and behavior responses were videotaped on pre-CCD 1 days and post-CCD 1, 3, 5, 7 days. The optimal concentration that led to a significant difference after CCD was determined and was used in the following in-vivoDRG imaging studies. Immunofluorescent staining was conducted to evaluate the expression of transient receptor potential vanilloid 1 (TRPV1) in DRG from na?ve and CCD mice. Results Behavioral tests showed that 0.1 g/L capsaicin elicits a significant difference in pain-like behaviors after CCD（n=8; post-CCD 1 day, P<0.01; post-CCD 5, 7 days P<0.01; post-CCD 3 days, P> 0.05. In vivocalcium imaging showed an enhanced number of activated DRG neurons to the injection of capsaicin in CCD mice, which was 75 in total of 398(n=4) for control mice and 169 in total of 382(n=6) (P<0.01). According to immunofluorescent staining results, there were 148 TRPV1+ neurons in total 653 counted neurons (n=10) for control mice and 237 TRPV1+ neurons in total of 611 neurons (n=6) for CCD mice (P<0.01). Conclusion Chronically compressed DRG neurons show upregulated TRPV1 receptor and enhanced responses to low-dose capsaicin, that produce pain hypersensitivity in the CCD mice.

Liver sinusoidal endothelial cells (LSECs) are gossamer-thin cells that line the hepatic sinusoid and they are perforated with pores called fenestrations clustered in sieve plates. There is growing evidence that fenestrations may work as a permselective ultrafiltration installation which is important for the hepatic to uptake substrates, particularly metabolism of lipoproteins. Abnormal fenestratel structure had been considered as a vital factor to liver lipid metabolism disorders. This review mainly focused on the relationship between ultrastructure of the fenestration, the fenestrated mechanism, the regulation factor of fenestration, and hepatic steatosis.

Osteoporosis (OP), a systemic bone metabolism disease, mainly manifested in the decrease of bone mass, the increase of bone fragility and the microstructure degeneration of the bone. Along with the in-depth research of the pathogenesis of osteoporosis, the imbalance differentiation of bone marrow mesenchymal stem cell (BMSCs) (Osteogenic differentiation decrease and adipogenic differentiation increase) is the main reason that causes osteoporosis. In this paper, we summarize the signal pathways of osteogenic differentiation and adipogenic differentiation of BMSCs. Better understand these signal pathways is conducive to elucidate and treat osteoporosis.