实验建立了高效液相色谱法检测丹田降脂丸中23-乙酰泽泻醇B等3种成分含量的测定方法。Capcell Pak UG C_(18)色谱柱分离;检测波长:葡糖苷、23-乙酰泽泻醇B和淫羊藿苷检测波长分别设定为319nm、208nm和271nm;柱温:28℃;进样体积:10μL;...实验建立了高效液相色谱法检测丹田降脂丸中23-乙酰泽泻醇B等3种成分含量的测定方法。Capcell Pak UG C_(18)色谱柱分离;检测波长:葡糖苷、23-乙酰泽泻醇B和淫羊藿苷检测波长分别设定为319nm、208nm和271nm;柱温:28℃;进样体积:10μL;以乙腈为流动相A,1.0%磷酸溶液为流动相B,梯度洗脱,洗脱方法:0~5min 13%A,5~15min 13%~45%A,15~24min 45%~86%A,24~30min 86%A,30~31min 13%A,30~35min 13%A;外标法定量检测。结果表明,葡糖苷、23-乙酰泽泻醇B和淫羊藿苷在0.1896~18.96、0.0983~9.83和0.0981~9.81μg/mL范围内线性良好;平均回收率分别为99.83%、99.46%和99.14%;精密度和重复性RSD(n=6)均在5.0%以内;供试品溶液在24h内稳定。该方法检测时间短、操作简单,可以用于丹田降脂丸的质量控制。展开更多
Herein,porous poly(lactic-co-glycolic acid)(PLGA)microspheres were prepared to load icariin andmiR-23b for the treatment of metastatic lung cancer.The microspheres exhibited desirable aerodynamic diameter,high drug lo...Herein,porous poly(lactic-co-glycolic acid)(PLGA)microspheres were prepared to load icariin andmiR-23b for the treatment of metastatic lung cancer.The microspheres exhibited desirable aerodynamic diameter,high drug loading and encapsulation efficiency,as well as a favorable drug release profile,which was beneficial for the deposition and exposure of drugs in the lung tissues.The release solution from microspheres exhibited a favorable anti-proliferative effect by inducting cell apoptosis and arresting the cell cycle at G1 phase,and meanwhile inhibited the migration and invasion of cancer cells.More importantly,the microspheres could be effectively inhaled and accumulated in the lung tissues to trigger the in situ apoptosis of tumor cells and suppress metastasis,using mice bearing melanoma-metastatic lung cancer as a model.Furthermore,inhalation of themicrospheres showed favorable biocompatibility,barely causing tissue damage.Overall,porous PLGA microspheres provide a promising platform for the inhalable co-delivery of drugs and genes to obtain ideal therapeutic efficacy in lung cancer and other pulmonary diseases.展开更多
目的探讨表达CD23的弥漫性大B细胞淋巴瘤(diffuse large B-cell lymphoma,DLBCL)的临床病理特点及可能的肿瘤相关免疫微环境。方法回顾性分析12例表达CD23的DLBCL临床病理资料,分析其临床、病理特点并研究其临床相关性及肿瘤相关免疫浸...目的探讨表达CD23的弥漫性大B细胞淋巴瘤(diffuse large B-cell lymphoma,DLBCL)的临床病理特点及可能的肿瘤相关免疫微环境。方法回顾性分析12例表达CD23的DLBCL临床病理资料,分析其临床、病理特点并研究其临床相关性及肿瘤相关免疫浸润。结果表达CD23的DLBCL约占所有DLBCL的9.45%;男女性各6例;平均发病年龄64.83岁;发生于淋巴结内者4例,结外者8例;9例为进展期(Ⅲ~Ⅳ期),3例为早期(Ⅰ~Ⅱ期);3例患者诊断后未经治疗且失访;1例患者手术后病情恶化死亡;8例患者经化疗后,2例死亡、1例进展、5例部分缓解。镜下肿瘤细胞均为弥漫浸润并破坏正常组织结构,可观察到肿瘤细胞呈现中心母细胞、免疫母细胞及间变性大细胞形态,其形态学均未见母细胞变及浆细胞样分化。Hans分型:除1例为GCB表型,其余11例均为非GCB表型。生物信息学研究发现CD23表达与调节性T细胞、NK细胞、浆细胞样树突细胞呈正相关,与中性粒细胞呈负相关。结论表达CD23的DLBCL患者主要为中老年人,以发生于淋巴结外为主,多为进展期(Ⅲ~Ⅳ期),随访结果显示其预后较差。形态学上相对于一般的DLBCL并无特殊,Hans分型提示肿瘤组织大多数为非GCB亚型,CD23表达对DLBCL的免疫微环境可能有一定的影响。展开更多
Background:Radiation sensitive 23 homolog B(RAD23B),a DNA repair-related protein,plays a contributory role in the development of multiple malignancies.This study aimed to explore the role of RAD23B in promoting colore...Background:Radiation sensitive 23 homolog B(RAD23B),a DNA repair-related protein,plays a contributory role in the development of multiple malignancies.This study aimed to explore the role of RAD23B in promoting colorectal cancer(CRC)metastasis and to elucidate the underlying molecular mechanisms.Methods:RAD23B was overexpressed in CRC cell lines SW480 and HCT-8,with empty vectors serving as controls.Invasion,cell proliferation,and migration were assessed using CCK-8 and Transwell assays.A xenograft mouse model was used to evaluate metastatic potential in vivo.Immunoprecipitation-mass spectrometry(IP-MS)and transcriptomic analysis by RNA sequencing(RNA-seq)were performed to identify signaling pathways regulated by RAD23B.Western blotting was used to analyze the expression of RAD23B,Talin1,Integrinsαv/β1,PI3K,p-PI3K,AKT,p-AKT,and MMP9.Immunohistochemistry was conducted to examine RAD23B and Integrinβ1 expression in CRC tissues.Results:RAD23B overexpression notably enhanced CRC migration,cell proliferation,and invasion both in vitro and in vivo.IP-MS,RNA-seq,and protein analysis revealed that RAD23B upregulated Talin1 and Integrinsαv/β1,resulting in an activation of the PI3K/AKT signaling pathway.Moreover,RAD23B promoted MMP9 expression,contributing to enhanced invasive potential.Conclusion:RAD23B facilitates CRCmetastasis through activation of the Talin1/Integrinαv/β1/PI3K/AKT/MMP9 signaling axis.These results provide novel insights into the role of RAD23B in CRC progression and identify it as a potential therapeutic target.展开更多
Microglia-mediated neuroinflammation plays a crucial role in ischemic stroke;consequently,understanding its regulation could facilitate the development of therapies for ischemic stroke.Chemerin 15,a 15-amino acid pept...Microglia-mediated neuroinflammation plays a crucial role in ischemic stroke;consequently,understanding its regulation could facilitate the development of therapies for ischemic stroke.Chemerin 15,a 15-amino acid peptide derived from chemerin,exerts powerful anti-inflammatory effects through ChemR23,modulates macrophage polarization,and diminishes inflammatory cytokine expression in peripheral inflammation models.However,its effects on microglia and stroke remain unclear.In this study,we used an in vitro oxygen/glucose deprivation BV2 cell model and a mouse model of ischemia-reperfusion injury to investigate the role of chemerin 15 in stroke and the underlying mechanisms.We co-cultured BV2 microglial cells with HT-22 hippocampal neurons and observed that chemerin 15 reduced apoptosis in HT-22 cells.Furthermore,we found that chemerin 15 binds to the ChemR23 receptor on the cell surface,inducing its internalization.This process regulated the activity of adenosine 5ʹ-monophosphate-activated protein kinase and inhibited its downstream target nuclear factor kappa B.These effects could be reversed by treatment with α-NETA,a ChemR23 inhibitor.In mice with ischemia-reperfusion injury,chemerin 15 modulated microglial polarization,reduced infarct volume and neuronal apoptosis,and facilitated cognitive and neurological function recovery.Our findings suggest that chemerin 15 suppresses the microglia-mediated inflammatory response,decreases neuronal apoptosis,and enhances long-term neurological function recovery by inducing ChemR23 internalization and regulating the adenosine 5ʹ-monophosphate-activated protein kinase/nuclear factor kappa B signaling pathway.展开更多
文摘实验建立了高效液相色谱法检测丹田降脂丸中23-乙酰泽泻醇B等3种成分含量的测定方法。Capcell Pak UG C_(18)色谱柱分离;检测波长:葡糖苷、23-乙酰泽泻醇B和淫羊藿苷检测波长分别设定为319nm、208nm和271nm;柱温:28℃;进样体积:10μL;以乙腈为流动相A,1.0%磷酸溶液为流动相B,梯度洗脱,洗脱方法:0~5min 13%A,5~15min 13%~45%A,15~24min 45%~86%A,24~30min 86%A,30~31min 13%A,30~35min 13%A;外标法定量检测。结果表明,葡糖苷、23-乙酰泽泻醇B和淫羊藿苷在0.1896~18.96、0.0983~9.83和0.0981~9.81μg/mL范围内线性良好;平均回收率分别为99.83%、99.46%和99.14%;精密度和重复性RSD(n=6)均在5.0%以内;供试品溶液在24h内稳定。该方法检测时间短、操作简单,可以用于丹田降脂丸的质量控制。
基金the National Natural Science Foundation of China(32271319 and 32071267)the Science and Technology Department of Jilin Province(YDZJ202301ZYTS537 and 20240402035GH)+1 种基金the Development and Reform Commission of Jilin Province(2023C015)the“Medicine+X”cross-innovation team of Bethune Medical Department of Jilin University“Leading the Charge with Open Competition”construction project(2022JBGS04).
文摘Herein,porous poly(lactic-co-glycolic acid)(PLGA)microspheres were prepared to load icariin andmiR-23b for the treatment of metastatic lung cancer.The microspheres exhibited desirable aerodynamic diameter,high drug loading and encapsulation efficiency,as well as a favorable drug release profile,which was beneficial for the deposition and exposure of drugs in the lung tissues.The release solution from microspheres exhibited a favorable anti-proliferative effect by inducting cell apoptosis and arresting the cell cycle at G1 phase,and meanwhile inhibited the migration and invasion of cancer cells.More importantly,the microspheres could be effectively inhaled and accumulated in the lung tissues to trigger the in situ apoptosis of tumor cells and suppress metastasis,using mice bearing melanoma-metastatic lung cancer as a model.Furthermore,inhalation of themicrospheres showed favorable biocompatibility,barely causing tissue damage.Overall,porous PLGA microspheres provide a promising platform for the inhalable co-delivery of drugs and genes to obtain ideal therapeutic efficacy in lung cancer and other pulmonary diseases.
文摘目的探讨表达CD23的弥漫性大B细胞淋巴瘤(diffuse large B-cell lymphoma,DLBCL)的临床病理特点及可能的肿瘤相关免疫微环境。方法回顾性分析12例表达CD23的DLBCL临床病理资料,分析其临床、病理特点并研究其临床相关性及肿瘤相关免疫浸润。结果表达CD23的DLBCL约占所有DLBCL的9.45%;男女性各6例;平均发病年龄64.83岁;发生于淋巴结内者4例,结外者8例;9例为进展期(Ⅲ~Ⅳ期),3例为早期(Ⅰ~Ⅱ期);3例患者诊断后未经治疗且失访;1例患者手术后病情恶化死亡;8例患者经化疗后,2例死亡、1例进展、5例部分缓解。镜下肿瘤细胞均为弥漫浸润并破坏正常组织结构,可观察到肿瘤细胞呈现中心母细胞、免疫母细胞及间变性大细胞形态,其形态学均未见母细胞变及浆细胞样分化。Hans分型:除1例为GCB表型,其余11例均为非GCB表型。生物信息学研究发现CD23表达与调节性T细胞、NK细胞、浆细胞样树突细胞呈正相关,与中性粒细胞呈负相关。结论表达CD23的DLBCL患者主要为中老年人,以发生于淋巴结外为主,多为进展期(Ⅲ~Ⅳ期),随访结果显示其预后较差。形态学上相对于一般的DLBCL并无特殊,Hans分型提示肿瘤组织大多数为非GCB亚型,CD23表达对DLBCL的免疫微环境可能有一定的影响。
基金supported by Hebei Natural Science Foundation(No.H2022105001)S&T Program of Hebei(No.22377727D).
文摘Background:Radiation sensitive 23 homolog B(RAD23B),a DNA repair-related protein,plays a contributory role in the development of multiple malignancies.This study aimed to explore the role of RAD23B in promoting colorectal cancer(CRC)metastasis and to elucidate the underlying molecular mechanisms.Methods:RAD23B was overexpressed in CRC cell lines SW480 and HCT-8,with empty vectors serving as controls.Invasion,cell proliferation,and migration were assessed using CCK-8 and Transwell assays.A xenograft mouse model was used to evaluate metastatic potential in vivo.Immunoprecipitation-mass spectrometry(IP-MS)and transcriptomic analysis by RNA sequencing(RNA-seq)were performed to identify signaling pathways regulated by RAD23B.Western blotting was used to analyze the expression of RAD23B,Talin1,Integrinsαv/β1,PI3K,p-PI3K,AKT,p-AKT,and MMP9.Immunohistochemistry was conducted to examine RAD23B and Integrinβ1 expression in CRC tissues.Results:RAD23B overexpression notably enhanced CRC migration,cell proliferation,and invasion both in vitro and in vivo.IP-MS,RNA-seq,and protein analysis revealed that RAD23B upregulated Talin1 and Integrinsαv/β1,resulting in an activation of the PI3K/AKT signaling pathway.Moreover,RAD23B promoted MMP9 expression,contributing to enhanced invasive potential.Conclusion:RAD23B facilitates CRCmetastasis through activation of the Talin1/Integrinαv/β1/PI3K/AKT/MMP9 signaling axis.These results provide novel insights into the role of RAD23B in CRC progression and identify it as a potential therapeutic target.
基金Gulin-Southwest Medical University Hospital Strategic Cooperation Project,No.2022 GLXNYDFY10(to JL)Suining First People’s Hospital-Southwest Medical University Cooperation Project,No.2021SNXNYD06(to JL)+2 种基金Postdoctoral Research Foundation of China,No.2021M692285(to LW)Key Research and Development Project of the Science and Technology Department of Sichuan Province,No.2022YFS0318(to LW)Post-Doctor Research Project of West China Hospital,Sichuan University,No.2021HXBH083(to LW).
文摘Microglia-mediated neuroinflammation plays a crucial role in ischemic stroke;consequently,understanding its regulation could facilitate the development of therapies for ischemic stroke.Chemerin 15,a 15-amino acid peptide derived from chemerin,exerts powerful anti-inflammatory effects through ChemR23,modulates macrophage polarization,and diminishes inflammatory cytokine expression in peripheral inflammation models.However,its effects on microglia and stroke remain unclear.In this study,we used an in vitro oxygen/glucose deprivation BV2 cell model and a mouse model of ischemia-reperfusion injury to investigate the role of chemerin 15 in stroke and the underlying mechanisms.We co-cultured BV2 microglial cells with HT-22 hippocampal neurons and observed that chemerin 15 reduced apoptosis in HT-22 cells.Furthermore,we found that chemerin 15 binds to the ChemR23 receptor on the cell surface,inducing its internalization.This process regulated the activity of adenosine 5ʹ-monophosphate-activated protein kinase and inhibited its downstream target nuclear factor kappa B.These effects could be reversed by treatment with α-NETA,a ChemR23 inhibitor.In mice with ischemia-reperfusion injury,chemerin 15 modulated microglial polarization,reduced infarct volume and neuronal apoptosis,and facilitated cognitive and neurological function recovery.Our findings suggest that chemerin 15 suppresses the microglia-mediated inflammatory response,decreases neuronal apoptosis,and enhances long-term neurological function recovery by inducing ChemR23 internalization and regulating the adenosine 5ʹ-monophosphate-activated protein kinase/nuclear factor kappa B signaling pathway.
