The role of basophils in asthma / 中华实用儿科临床杂志

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.

Advances in the study of susceptibility genes to bronchial asthma in children Table 1 Genome-wide association study found some new bronchial asthma and related phenotype genes in recent years / 中华实用儿科临床杂志

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.

Holistic integrative medicine for childhood allergic diseases / 中华实用儿科临床杂志

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.

Holistic integrative medicine for childhood allergic diseases / 中华实用儿科临床杂志

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.

Effect of Sinomenine on Expression of COX2, α7nAChR and A2A in A549 Cells / 广州中医药大学学报

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.

Total glucosides of paeony inhibits adriamycin-induced nephropathy in rats through blocking TLR4/NF-κB/TGF-β1 signaling / 中国生化药物杂志

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.