目的:观察龙牙楤木总皂苷(As)对心肌缺血动物及心肌细胞形态、搏动频率和存活率的影响。方法:采用异丙肾上腺素(Iso)致动物急性心肌缺血的方法,观察 As 对注射 Iso 后心肌组织结构、超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量、血清中5...目的:观察龙牙楤木总皂苷(As)对心肌缺血动物及心肌细胞形态、搏动频率和存活率的影响。方法:采用异丙肾上腺素(Iso)致动物急性心肌缺血的方法,观察 As 对注射 Iso 后心肌组织结构、超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量、血清中5-羟色胺(5-HT)、去甲肾上腺素(Lev)含量的影响;采用原代培养大鼠心肌细胞技术,观察 As 对心肌细胞形态、搏动频率和存活率的影响。结果:As 对 Iso 所致大鼠心肌坏死有较好的防治作用,保护心肌组织中 SOD 活性,降低心肌组织中MDA 含量及血清中5-HT 和 Lev 含量;体外试验显示,加入 As 后心肌细胞搏动幅度明显增大,30.0μg/mL 组可增加心肌细胞的存活率。结论:As 对 Iso 所致的急性心肌缺血,具有明显保护作用;对心肌细胞具有正性肌力,负性变时效应,As 30.0μg/mL 时对心肌细胞具有明显保护作用。展开更多
Group 2 innate lymphoid cells(ILC2s)are a category of heterogeneous cells that produce the cytokines IL-5 and IL-13,which mediate the type 2 immune response.However,specific drug targets on lung ILC2s have rarely been...Group 2 innate lymphoid cells(ILC2s)are a category of heterogeneous cells that produce the cytokines IL-5 and IL-13,which mediate the type 2 immune response.However,specific drug targets on lung ILC2s have rarely been reported.Previous studies have shown that type 2 cytokines,such as IL-5 and IL-13,are related to depression.Here,we demonstrated the negative correlation between the depression-associated monoamine neurotransmitter serotonin and secretion of the cytokines IL-5 and IL-13 by ILC2s in individuals with depression.Interestingly,serotonin ameliorates papain-induced lung inflammation by suppressing ILC2 activation.Our data showed that the serotonin receptor HTR2A was highly expressed on ILC2s from mouse lungs and human PBMCs.Furthermore,an HTR2A selective agonist(DOI)impaired ILC2 activation and alleviated the type 2 immune response in vivo and in vitro.Mice with ILC2-specific depletion of HTR2A(Il5^(cre/+)·Htr2a^(flox/flox)mice)abolished the DOI-mediated inhibition of ILC2s in a papain-induced mouse model of inflammation.In conclusion,serotonin and DOI could restrict the type 2 lung immune response,indicating a potential treatment strategy for type 2 lung inflammation by targeting HTR2A on ST2+ILC2s.展开更多
文摘目的:观察龙牙楤木总皂苷(As)对心肌缺血动物及心肌细胞形态、搏动频率和存活率的影响。方法:采用异丙肾上腺素(Iso)致动物急性心肌缺血的方法,观察 As 对注射 Iso 后心肌组织结构、超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量、血清中5-羟色胺(5-HT)、去甲肾上腺素(Lev)含量的影响;采用原代培养大鼠心肌细胞技术,观察 As 对心肌细胞形态、搏动频率和存活率的影响。结果:As 对 Iso 所致大鼠心肌坏死有较好的防治作用,保护心肌组织中 SOD 活性,降低心肌组织中MDA 含量及血清中5-HT 和 Lev 含量;体外试验显示,加入 As 后心肌细胞搏动幅度明显增大,30.0μg/mL 组可增加心肌细胞的存活率。结论:As 对 Iso 所致的急性心肌缺血,具有明显保护作用;对心肌细胞具有正性肌力,负性变时效应,As 30.0μg/mL 时对心肌细胞具有明显保护作用。
基金the Ministry of Science and Technology of China(2018YFA0507402)the National Natural Science Foundation of China(32000667)+5 种基金the Shanghai Science and Technology Innovation Action(21ZR1470600)the Youth Innovation Promotion Association of the Chinese Academy of Sciences(2022264)the National Natural Science Foundation of China(81771465 and 81930033)the Science and Technology Project of the Department of Education of Jiangxi Province(GJJ211248)the Division of Intramural Research,National Institute of Allergy and Infectious Diseases,National Institutes of Health(grant 1ZIA-Al-001169)the US-China Biomedical Collaborative Research Program(grant Al-129775).
文摘Group 2 innate lymphoid cells(ILC2s)are a category of heterogeneous cells that produce the cytokines IL-5 and IL-13,which mediate the type 2 immune response.However,specific drug targets on lung ILC2s have rarely been reported.Previous studies have shown that type 2 cytokines,such as IL-5 and IL-13,are related to depression.Here,we demonstrated the negative correlation between the depression-associated monoamine neurotransmitter serotonin and secretion of the cytokines IL-5 and IL-13 by ILC2s in individuals with depression.Interestingly,serotonin ameliorates papain-induced lung inflammation by suppressing ILC2 activation.Our data showed that the serotonin receptor HTR2A was highly expressed on ILC2s from mouse lungs and human PBMCs.Furthermore,an HTR2A selective agonist(DOI)impaired ILC2 activation and alleviated the type 2 immune response in vivo and in vitro.Mice with ILC2-specific depletion of HTR2A(Il5^(cre/+)·Htr2a^(flox/flox)mice)abolished the DOI-mediated inhibition of ILC2s in a papain-induced mouse model of inflammation.In conclusion,serotonin and DOI could restrict the type 2 lung immune response,indicating a potential treatment strategy for type 2 lung inflammation by targeting HTR2A on ST2+ILC2s.
