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ObjectiveTo investigate the antidepressant effect of Sinisan （SNS） by regulating glycogen aynthase kinase-3β （GSK-3β）/tumor necrosis factor alpha-induced protein 3（A20）/CCAAT enhancer binding protein β（C/EBPβ） to inhibit the activation of microglia. MethodA total of 72 male C57/6J mice were randomly divided into the normal group， model group， fluoxetine group （5.0 mg·kg-1）， low-dose Sinisan group （4.9 g·kg-1）， medium-dose Sinisan group （9.8 g·kg-1）， and high-dose Sinisan group （19.6 g·kg-1）， with 12 mice in each group. After one week of adaptive feeding， chronic unpredictable mild stress （CUMS） was performed to establish the depression model. In the fifth week， drug treatment was conducted for four weeks. In the ninth week， behavioral tests were performed， including sucrose preference test （SPT）， open field test （OPT）， elevated plus maze （EPM） test， and forced swimming test （FST）. Western blot was used to detect the expression levels of interleukin-1β （IL-1β）， interleukin-6 （IL-6）， nitric oxide synthase （iNOS）， GSK-3β， A20， and C/EBPβ in the cortex. The expression of M1-polarized ionized calcium-binding adapter molecule 1 （Iba1） and cluster of differentiation 68 （CD68） in microglia was detected by immunofluorescence. ResultAfter eight weeks of CUMS， compared with the normal group， the mice in the model group had a significantly reduced sucrose preference rate （P<0.01）， and the activity in the central area of the OPT was significantly reduced （P<0.01）. The activity in the open arm area of the EPM test was significantly reduced （P<0.05）， and the immobility time of FST was increased （P<0.01）. The expression levels of inflammatory proteins IL-1β， IL-6， and iNOS were increased （P<0.01）， and the fluorescence co-localization index of Iba1 and CD68 was increased （P<0.05）. The protein expression levels of GSK-3β and C/EBPβ were significantly increased （P<0.05， P<0.01）. After four weeks of SNS intervention， compared with the model group， the mice in the SNS group had significantly increased sucrose preference rate （P<0.01）， significantly increased activities in the central area and the open arm area in the OPT and the EPM test （P<0.05）， and significantly reduced immobility time in the FST （P< 0.01）. The protein expression levels of IL-1β， IL-6， and iNOS were significantly decreased （P<0.05）， and the fluorescence co-localization index of Iba1 and CD68 was decreased in the high-dose SNS group （P<0.05）. The protein expression levels of GSK-3β and C/EBPβ in the medium-dose and high-dose SNS groups were significantly decreased （P<0.01）， and that of A20 was significantly increased （P<0.01）. ConclusionThe antidepressant effect of SNS is related to the regulation of GSK-3β/A20/C/EBPβ protein expression and the inhibition of M1-type activation of microglia.
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Basophils have been neglected for a long time as an immune cell.Recently, it gained respect because of its important role in helper T lymphocytes(Th)2 immune response.Basophils are involved in the pathogenesis of bronchial asthma through a variety of possible mechanisms.Basophils can act as initiators initiate and establish Th2 immune response by interacting with dendritic cells; basophils can act as immune regulators, regulate immune cell functions such as type 2 innate lymphoid cells by secreting cytokines such as interleukin 4 to consolidate allergic inflammation; basophils can also act as immune effectors participate in allergic airway inflammation through IgE-depended and non IgE-depended activation.In addition, clinical research is focused on the usage of basophil activation status as possible biomarker in predicting the outcome of allergic disease therapy, which is of great clinic value in individualized management of asthma.
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Bronchial asthma(asthma for short)is a complex heterogeneous disease,which is caused by multi-ple gene-environmental interaction. With the progress of asthma gene research,some new childhood asthma suscepti-bility genes have been found,and the influence of genes interaction with environment on asthma is being widely atten-ded;different genetic loci combination can predict the onset of childhood asthma. Now,the history of asthma gene re-search and some newly discovered childhood asthma susceptibility genes in recent years and different genetic loci com-bination prediction effect and so on were introduced.
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The prevalence of allergic diseases in children have increased year by year recently.Although the clinical manifestations of childhood allergic diseases are various, their pathogenesis is nearly the same.In the meantime, childhood allergic diseases are combined with nutritional, psychological, spiritual and family social problems, which if not solved properly will affect the allergic diseases themselves.Therefore, it is necessary to apply the concept of holistic integrated medicine and integrate multiple related departments to solve the problem of allergy, which is patient-oriented.This article introduces the necessity and approaches for integration of childhood allergic diseases.
RÉSUMÉ
The prevalence of allergic diseases in children have increased year by year recently.Although the clinical manifestations of childhood allergic diseases are various,their pathogenesis is nearly the same.In the meantime,childhood allergic diseases are combined with nutritional,psychological,spiritual and family social problems,which if not solved properly will affect the allergic diseases themselves.Therefore,it is necessary to apply the concept of holistic integrated medicine and integrate multiple related departments to solve the problem of allergy,which is patient-oriented.This article introduces the necessity and approaches for integration of childhood allergic diseases.
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Objective To observe the effect of sinomenine (SIN) on the expression of cyclooxygenase (COX2),alpha-7 nicotinic acetylcholine receptor(α7nAChR) and adenosine receptor(A2A) in A549 cells,and to explore the relative mechanism for cell proliferation.Methods The effect of SIN and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) on the proliferation of A549 cells was determined by methyl thiazolyl tetrazolium (MTT) assay.The effect of SIN and NNK on the migration of A549 cells was detected by cell wound scratch assay.The effect of SIN and NNK on COX2 expression in A549 cells was determined by Western blotting method.The effect of SIN and NNK on the expression of α7nAChR and A2A mRNA and protein was evaluated by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting method.Results NNK increased the proliferation and migration of A549 cells,while SIN inhibited the proliferation and migration of A549 cells.COX2 expression level was increased in NNK group but was decreased in SIN group.The expression levels of α7nAChR and A2A were up-regulated in NNK group but were down-regulated in SIN group.Conclusion SIN plays a role in inhibiting the proliferation and migration of A549 cells by suppressing COX2 expression.SIN has an inhibitory effect on the expression of α7nAChR and A2A.
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Objective To study effect and its possible mechanism of total glucosides of paeony ( TGP ) on adriamycin-induced nephropathy rats.Methods Thirty male SD rats were randomly divided into normal group ( CON) , adriamycin-induced nephropathy group ( ADRN) and TGP-treated ADRN group (TGP).The rat nephropathy model was established by adriamycin injection.At the end of the 8th week after treatment, ELISA was used to detect the level of Cr and BUN.The values of 24 urine protein was determined by urinary protein kit.Masson staining was used to observe the fibrosis.RT-PCR was used to detect the mRNA levels of TLR4/NF-κB/TGF-β1 .Immunohistochemical method was used to detect the content of TLR4/NF-κB/TGF-β1.ResuIts Compared with the CON group, the level of Cr, BUN, 24 urine protein of ADRN group rised(P<0.01), the degree of fibrosis of ADRN group were aggravated(P<0.01), and the expressions of TLR4/NF-κB/TGF-β1 of ADRN group increased significantly.However, compared with ADRN group, the(P<0.01) level of Cr, BUN, 24 urine protein of TGP-treated rats reduced(P<0.01), the degree of fibrosis of TGP-treated rats eased(P<0.05), and the expressions of TLR4/NF-κB/TGF-β1 of TGP-treated rats decreased significantly.ConcIusion TGP retards the process of fibrosis and reduces the pathological damage in adriamycin-induced rats by down-regulating the expression of TLR4/NF-κB/TGF-β1 signaling.