该文研究羊肚菌蛋白水解物(morchella protein hydrolysate,MPH)及其硒化衍生物(Se-MPH)的细胞保护作用和安全性。利用H_(2)O_(2)诱导的Caco-2细胞氧化损伤模型研究了MPH和Se-MPH的细胞保护作用。结果显示,MPH和Se-MPH可通过减轻氧化应...该文研究羊肚菌蛋白水解物(morchella protein hydrolysate,MPH)及其硒化衍生物(Se-MPH)的细胞保护作用和安全性。利用H_(2)O_(2)诱导的Caco-2细胞氧化损伤模型研究了MPH和Se-MPH的细胞保护作用。结果显示,MPH和Se-MPH可通过减轻氧化应激和抑制细胞凋亡来保护Caco-2细胞免受氧化损伤,这种保护作用可能主要归因于Nrf2信号通路的激活和凋亡相关蛋白表达的调节。通过细胞毒性试验、红细胞溶血实验、细菌回复突变(bacterial reverse mutation,Ames)试验以及鸡胚绒毛尿囊膜(chick embryo chorioallantoic membrane,CAM)试验研究了MPH和Se-MPH的安全性。结果证实,MPH和Se-MPH没有细胞毒性、溶血活性和致突变潜力,在CAM实验中未观察到明显的血管形态学变化及出血现象。所有这些研究表明,MPH和Se-MPH具有显著的细胞保护作用和良好的安全性,有望作为潜在的营养性、功能性或药物性成分得到开发利用。展开更多
Objective:The neurotoxicity of carbon monoxide(CO)to the central nervous system is a key pathogenesis of delayed encephalopathy after acute carbon monoxide poisoning(DEACMP).Our previous study found that retinoic acid...Objective:The neurotoxicity of carbon monoxide(CO)to the central nervous system is a key pathogenesis of delayed encephalopathy after acute carbon monoxide poisoning(DEACMP).Our previous study found that retinoic acid(RA)can suppress the neurotoxic effects of CO.This study further explores,in vivo and in vitro,the molecular mechanisms by which RA alleviates CO-induced central nervous system damage.Methods:A cytotoxic model was established using the mouse hippocampal neuronal cell line HT22 and primary oligodendrocytes exposed to CO,and a DEACMP animal model was established in adult Kunming mice.Cell viability and apoptosis of hippocampal neurons and oligodendrocytes were assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)assay and Annexin V/propidium iodide(PI)double staining.The transcriptional and protein expression of each gene was detected using real time fluorescence quantitative PCR(RT-qPCR)and Western blotting.Long noncoding RNA(lncRNA)SNHG15 and LINGO-1 were knocked down or overexpressed to observe changes in neurons and oligodendrocytes.In DEACMP mice,SNHG15 or LINGO-1 were knocked down to assess changes in central nervous tissue and downstream protein expression.Results:RA at 10 and 20μmol/L significantly reversed CO-induced apoptosis of hippocampal neurons and oligodendrocytes,downregulation of SNHG15 and LINGO-1,and upregulation of brain-derived neurotrophic factor(BDNF)and tyrosine kinase receptor B(TrkB)(all P<0.05).Overexpression of SNHG15 or LINGO-1 weakened the protective effect of RA against CO-induced cytotoxicity(all P<0.05).Knockdown of SNHG15 or LINGO-1 alleviated CO-induced apoptosis of hippocampal neurons and oligodendrocytes and upregulated BDNF and TrkB expression levels(all P<0.05).Experiments in DEACMP model mice showed that knockdown of SNHG15 or LINGO-1 mitigated central nervous system injury in DEACMP(all P<0.05).Conclusion:RA alleviates CO-induced apoptosis of hippocampal neurons and oligodendrocytes,thereby reducing central nervous system injury and exerting neuroprotective effects.LncRNA SNHG15 and LINGO-1 are key molecules mediating RA induced inhibition of neuronal apoptosis and are associated with the BDNF/TrkB pathway.These findings provide a theoretical framework for optimizing the clinical treatment of DEACMP and lay an experimental foundation for elucidating its molecular mechanisms.展开更多
It aims to investigate the protective effects of sodium hyaluronate,panthenol,Portulaca oleracea L.and Calendula officinalis L.on hyperosmotic dehydration-induced injury of human immortalized keratinocytes(HaCaT).The ...It aims to investigate the protective effects of sodium hyaluronate,panthenol,Portulaca oleracea L.and Calendula officinalis L.on hyperosmotic dehydration-induced injury of human immortalized keratinocytes(HaCaT).The safety mass concentrations of four raw materials were screened by detecting cell viability,and the secretion of hyaluronic acid(HA)was determined using the ELISA method.The expression of HaCaT barrier function related genes(OVOL1,EREG,TGM1,TGM2,IVL,IRF6,THBS1,CASP14)was detected at the mRNA level to explore the regulatory effect of four raw materials on these genes.The results demonstrate that pretreatment with the four kinds of raw materials could increase the cell viability after hyperosmotic dehydration,promote the secretion of HA,and improve the expression of barrier function related genes after hyperosmotic dehydration,among which panthenol and Calendula officinalis L.are better.The results show that the four raw materials have a certain protective effect on the hyperosmotic dehydration cell model,which provides data support for its application in cosmetics.展开更多
文摘目的研究姜黄素(Curcumin)对于血红素加氧酶-1(heme oxygenase-1,HO-1)和核因子相关因子2(nuclear factor erythroid2-related factor2,Nrf-2)表达的影响,探讨Curcumin保护神经细胞的作用机制。方法 SH-SY5Y(人神经母细胞瘤)细胞用0、1.25、5.0、20.0μmol·L-1 Curcumin处理24h,以及用5.0μmol·L-1 Curcumin分别处理细胞0、12、24、48h,然后用RT-PCR和Western blot检测各组的mRNA和蛋白的表达,并在各个浓度组使用Nrf-2siRNA,Western blot检测转染Nrf-2siRNA后HO-1的表达情况。结果 Curcumin处理后,SH-SY5Y细胞中Nrf-2和HO-1的表达均明显增强,且呈时间和浓度依赖性(P<0.05),0、1.25、5.0、20.0μmol·L-1 Curcumin处理的细胞24h后HO-1表达与用0,1.25,5.0,20.0μmol·L-1 Curcumin和转染Nrf-2siRNA同时处理24h后的细胞HO-1表达相比明显下降(group 1 vs group 5,group 2 vs group 6,group 3 vsgroup 7,group 4 vs group 8,P<0.05)。结论 Curcumin通过Nrf-2诱导HO-1的表达作用,可能是其抑制神经细胞氧化应激、发挥保护作用的机制之一。
基金supported by the Natural Science Foundation of Hunan Province(2021JJ31089)the Scientific Research Project of Health Commission of Hunan Province(202203104548),China。
文摘Objective:The neurotoxicity of carbon monoxide(CO)to the central nervous system is a key pathogenesis of delayed encephalopathy after acute carbon monoxide poisoning(DEACMP).Our previous study found that retinoic acid(RA)can suppress the neurotoxic effects of CO.This study further explores,in vivo and in vitro,the molecular mechanisms by which RA alleviates CO-induced central nervous system damage.Methods:A cytotoxic model was established using the mouse hippocampal neuronal cell line HT22 and primary oligodendrocytes exposed to CO,and a DEACMP animal model was established in adult Kunming mice.Cell viability and apoptosis of hippocampal neurons and oligodendrocytes were assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)assay and Annexin V/propidium iodide(PI)double staining.The transcriptional and protein expression of each gene was detected using real time fluorescence quantitative PCR(RT-qPCR)and Western blotting.Long noncoding RNA(lncRNA)SNHG15 and LINGO-1 were knocked down or overexpressed to observe changes in neurons and oligodendrocytes.In DEACMP mice,SNHG15 or LINGO-1 were knocked down to assess changes in central nervous tissue and downstream protein expression.Results:RA at 10 and 20μmol/L significantly reversed CO-induced apoptosis of hippocampal neurons and oligodendrocytes,downregulation of SNHG15 and LINGO-1,and upregulation of brain-derived neurotrophic factor(BDNF)and tyrosine kinase receptor B(TrkB)(all P<0.05).Overexpression of SNHG15 or LINGO-1 weakened the protective effect of RA against CO-induced cytotoxicity(all P<0.05).Knockdown of SNHG15 or LINGO-1 alleviated CO-induced apoptosis of hippocampal neurons and oligodendrocytes and upregulated BDNF and TrkB expression levels(all P<0.05).Experiments in DEACMP model mice showed that knockdown of SNHG15 or LINGO-1 mitigated central nervous system injury in DEACMP(all P<0.05).Conclusion:RA alleviates CO-induced apoptosis of hippocampal neurons and oligodendrocytes,thereby reducing central nervous system injury and exerting neuroprotective effects.LncRNA SNHG15 and LINGO-1 are key molecules mediating RA induced inhibition of neuronal apoptosis and are associated with the BDNF/TrkB pathway.These findings provide a theoretical framework for optimizing the clinical treatment of DEACMP and lay an experimental foundation for elucidating its molecular mechanisms.
文摘It aims to investigate the protective effects of sodium hyaluronate,panthenol,Portulaca oleracea L.and Calendula officinalis L.on hyperosmotic dehydration-induced injury of human immortalized keratinocytes(HaCaT).The safety mass concentrations of four raw materials were screened by detecting cell viability,and the secretion of hyaluronic acid(HA)was determined using the ELISA method.The expression of HaCaT barrier function related genes(OVOL1,EREG,TGM1,TGM2,IVL,IRF6,THBS1,CASP14)was detected at the mRNA level to explore the regulatory effect of four raw materials on these genes.The results demonstrate that pretreatment with the four kinds of raw materials could increase the cell viability after hyperosmotic dehydration,promote the secretion of HA,and improve the expression of barrier function related genes after hyperosmotic dehydration,among which panthenol and Calendula officinalis L.are better.The results show that the four raw materials have a certain protective effect on the hyperosmotic dehydration cell model,which provides data support for its application in cosmetics.
