AIM:To characterize effect of astaxanthin(ASX)in Aspergillus fumigatus(A.fumigatus)induced keratitis in mouse model.METHODS:In vivo,fungal keratitis mouse model was established in C57BL/6 mice using A.fumigatus,follow...AIM:To characterize effect of astaxanthin(ASX)in Aspergillus fumigatus(A.fumigatus)induced keratitis in mouse model.METHODS:In vivo,fungal keratitis mouse model was established in C57BL/6 mice using A.fumigatus,followed by ASX or dimethyl sulfoxide(DMSO)treatment.Clinical responses were evaluated by clinical score and myeloperoxidase(MPO)assay.Inflammatory cytokines were assessed by reverse-transcription polymerase chain reaction(RT-PCR),Western blot,immunofluorescence,and enzyme-linked immuno sorbent assay(ELISA).RESULTS:In animal model,ASX improved corneal transparency and clinical response,suppressed the expression of inflammatory cytokine like IL-1β,TNF-α,and HMGB-1.Neutrophil levels have been shown to decrease in ASX-treated cornea by immunofluorescence and MPO.TLR2 and TLR4 levels were lower in ASX-treated group than DMSO-treated.CONCLUSION:ASX can suppress inflammatory response and reduce inflammatory cytokine production in mice model with A.fumigatus keratitis.展开更多
Pancreatic ductal adenocarcinoma(PDAC)is one of the most lethal neoplasms worldwide and represents the vast majority of pancreatic cancer cases.Understanding the molecular pathogenesis and the underlying mechanisms in...Pancreatic ductal adenocarcinoma(PDAC)is one of the most lethal neoplasms worldwide and represents the vast majority of pancreatic cancer cases.Understanding the molecular pathogenesis and the underlying mechanisms involved in the initiation,maintenance,and progression of PDAC is an urgent need,which may lead to the development of novel therapeutic strategies against this deadly cancer.Here,we review the role of SET and MYND domaincontaining protein 2(SMYD2)in initiating and maintaining PDAC development through methylating multiple tumor suppressors and oncogenic proteins.Given the broad substrate specificity of SMYD2 and its involvement in diverse oncogenic signaling pathways in many other cancers,the mechanistic extrapolation of SMYD2 from these cancers to PDAC may allow for developing new hypotheses about the mechanisms driving PDAC tumor growth and metastasis,supporting a proposition that targeting SMYD2 could be a powerful strategy for the prevention and treatment of PDAC.展开更多
基金Supported by the National Natural Science Foundation of China(No.81870632)Youth Project of Natural Science Foundation of ghandong Province(No.ZR2019BH004).
文摘AIM:To characterize effect of astaxanthin(ASX)in Aspergillus fumigatus(A.fumigatus)induced keratitis in mouse model.METHODS:In vivo,fungal keratitis mouse model was established in C57BL/6 mice using A.fumigatus,followed by ASX or dimethyl sulfoxide(DMSO)treatment.Clinical responses were evaluated by clinical score and myeloperoxidase(MPO)assay.Inflammatory cytokines were assessed by reverse-transcription polymerase chain reaction(RT-PCR),Western blot,immunofluorescence,and enzyme-linked immuno sorbent assay(ELISA).RESULTS:In animal model,ASX improved corneal transparency and clinical response,suppressed the expression of inflammatory cytokine like IL-1β,TNF-α,and HMGB-1.Neutrophil levels have been shown to decrease in ASX-treated cornea by immunofluorescence and MPO.TLR2 and TLR4 levels were lower in ASX-treated group than DMSO-treated.CONCLUSION:ASX can suppress inflammatory response and reduce inflammatory cytokine production in mice model with A.fumigatus keratitis.
文摘Pancreatic ductal adenocarcinoma(PDAC)is one of the most lethal neoplasms worldwide and represents the vast majority of pancreatic cancer cases.Understanding the molecular pathogenesis and the underlying mechanisms involved in the initiation,maintenance,and progression of PDAC is an urgent need,which may lead to the development of novel therapeutic strategies against this deadly cancer.Here,we review the role of SET and MYND domaincontaining protein 2(SMYD2)in initiating and maintaining PDAC development through methylating multiple tumor suppressors and oncogenic proteins.Given the broad substrate specificity of SMYD2 and its involvement in diverse oncogenic signaling pathways in many other cancers,the mechanistic extrapolation of SMYD2 from these cancers to PDAC may allow for developing new hypotheses about the mechanisms driving PDAC tumor growth and metastasis,supporting a proposition that targeting SMYD2 could be a powerful strategy for the prevention and treatment of PDAC.
