检索结果-南通市图书馆

Moxibustion of Zusanli(ST36)and Shenshu(BL23)alleviates the inflammation of rheumatoid arthritis in rats through regulating macrophage migration inhibitory factor/glucocorticoids signaling

引用

Journal of Traditional Chinese Medicine 2024年第2期44卷 353-361页

作者： ZHANG Linlin ZHONG Yumei LU Wenting SHANG Yanan GUO Yanding LUO Xiaochao CHEN Yang LUO Kun HU Danhui YU Huiling ZHOU Haiyan Acupuncture and Moxibustion College Chengdu University of Traditional Chinese MedicineChengdu 610075China Department of Painology First People's Hospital of ChengduChengdu 610095China Chinese Evidence-Based Medicine Centre West China HospitalSichuan UniversityChengdu 610044China Traditional Chinese Medicine College Chongqing Medical UniversityChongqing 400016China External treatment center First People's Hospital of ChengduChengdu 610095China

OBJECTIVE:To test the hypothesis that moxibustion may inhibit rheumatoid arthritis(RA)synovial inflammation by regulating the expression of macrophage migration inhibitory factor(MIF)/glucocorticoids(GCs).METHODS:Fifty male Sprague-Dawley rats were randomly divided into five groups(n=10 each):blank Control(CON)group,RA Model(RA)group,Moxibustion(MOX)group,MIF inhibitor(S,R)-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid methyl ester(ISO-1)group,and Moxibustion+MIF inhibitor ISO-1(MOX+ISO-1)*** in the ISO-1 group and ISO-1+MOX group were intraperitoneally injected with the inhibitor *** rats in the RA group,ISO-1 group,MOX group,and ISO-1+MOX group were injected with Freund's complete adjuvant(FCA)in the right hind footpad to establish an experimental RA rat *** the MOX group and MOX+ISO-1 group,rats were treated with *** thickness of the footpads of the rats in each group was measured at three-time points before,after modeling and after moxibustion *** contents of serum MIF,corticosterone(CORT),tumor necrosis factor-α(TNF-α)and interleukin-1β(IL-1β)were detected by enzyme-linked immunosorbent assay;and the contents of synovial MIF were detected by Western ***-eosin(HE)staining method was used to observe the pathological changes of synovial tissue under a section light microscope,and pathological scoring was performed according to the grading standard of the degree of synovial tissue ***:Moxibustion was found to reduce the level of MIF and alleviate inflammation in RA rats in this *** addition,after inhibiting the expression of MIF,the level of CORT increased,and the level of TNF-α *** RA rats with inhibited MIF by moxibustion,the level of CORT was almost unchanged,but the level of TNF-α further *** correlation analysis data suggested that MIF was positively related to the expression of TNF-α and negatively correlated with the expression of ***:Reducing MIF to

关键词： rheumatoid arthritis macrophage migration inhibitory factor moxibustion corticosterone glucocorticoids

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

The roles of macrophage migration inhibitory factor in retinal diseases

引用

Neural Regeneration Research 2024年第2期19卷 309-315页

作者： Hongbing Zhang Xianjiao Zhang Hongsong Li Bing Wang Pei Chen Jiamin Meng Shaanxi Institute of Ophthalmology Xi’anShaanxi ProvinceChina Department of Ophthalmology First Affiliated Hospital of Northwest UniversityXi’anShaanxi ProvinceChina Department of Pathology First Affiliated Hospital of Northwest UniversityXi’anShaanxi ProvinceChina

macrophage migration inhibitory factor(MIF),a multifunctional cytokine,is secreted by various cells and participates in inflammatory reactions,including innate and adaptive *** are some evidences that MIF is involved in many vitreoretinal *** example,MIF can exacerbate many types of uveitis;measurements of MIF levels can be used to monitor the effectiveness of uveitis *** also alleviates trauma-induced and glaucoma-induced optic nerve ***,MIF is critical for retinal/choroidal neovascularization,especially complex *** exacerbates retinal degeneration;thus,anti-MIF therapy may help to mitigate retinal *** protects uveal melanoma from attacks by natural killer *** mechanism underlying the effects of MIF in these diseases has been demonstrated:it binds to cluster of differentiation 74,inhibits the c-Jun N-terminal kinase pathway,and triggers mitogen-activated protein kinases,extracellular signal-regulated kinase-1/2,and the phosphoinositide-3-kinase/Akt *** also upregulates Toll-like receptor 4 and activates the nuclear factor kappa-B signaling *** review focuses on the structure and function of MIF and its receptors,including the effects of MIF on uveal inflammation,retinal degeneration,optic neuropathy,retinal/choroidal neovascularization,and uveal melanoma.

关键词： diabetic retinopathy glaucoma macrophage migration inhibitory factor migration inhibitory factor receptor optic neuropathy retinal degeneration retinal neovascular uveal melanoma uveitis

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

macrophage migration inhibitory factor regulates proliferation of gastric cancer cells via the PI3K/Akt pathway

引用

World Journal of Gastroenterology 2009年第44期15卷 5541-5548页

作者： Guo-Qing Li Juan Xie Xiao-Yong Lei Li Zhang Department of Gastroenterology The Second Affiliated Hospital University of South China Hengyang 421001 Hunan Province China Institute of Pharmacy and Pharmacology University of South China Hengyang 421001 Hunan Province China

AIM:To investigate the effects of macrophage migration inhibitory factor (MIF) on proliferation of human gastric cancer MGC-803 cells and expression of cyclin D1 and p27Kip1 in them,and further determine whether the effects are related to the PI3K/Akt signal transduction pathway. METHODS:Gastric cancer MGC-803 cells were cultured and then treated with 50 μg/L recombinant human MIF (rhMIF) with and without a PI3K inhibitor,LY294002 (25 μmol/L). MTT assay was used to detect the prolifer-ation of MGC-803 cells. Cell cycle was detected by flow cytometry. Expression of cyclin D1 and p27Kip1 mRNA was by reverse transcription-polymerase chain reaction. Protein expression of phosphorylated Akt (p-Akt),Akt,cyclin D1 and p27Kip1 was examined by immunocyto-chemistry and Western blotting. RESULTS:rhMIF signifi cantly stimulated the prolifera-tion of MGC-803 cells and cell cycle progression from G1 phase to S phase in a concentration-and time-de-pendent manner. After the MGC-803 cells were treated with rhMIF for 24 h,the expression of cyclin D1 was signifi cantly up-regulated compared with the cells not treated with rhMIF at both mRNA and protein levels(0.97 ± 0.02 vs 0.74 ± 0.01,P = 0.002; 0.98 ± 0.05 vs 0.69 ± 0.04,P = 0.003). The p27Kip1 was down-regulated but only statistically significant at the protein level. rhMIF significantly increased the expression of p-Akt,which reached the peak at 30 min,but did not affect the expression of Akt. However,LY294002 inhibited all the effects of ***:macrophage MIF increases the proliferation of gastric cancer cells,induces the expression of cyclin D1 at the transcriptional level and inhibits the expression of p27Kip1 at the post-transcriptional level via the PI3K/Akt pathway.

关键词： macrophage migration inhibitory factor Gastric cancer Proliferation Cell cycle Cyclin D1 p27^Kip1 PI3K/Akt

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

macrophage migration inhibitory factor promotes the expression of GLUT4 glucose transporter through MEF2 and Zac1 in cardiomyocytes

引用

South China Journal of Cardiology 2015年第1期16卷 28-36页

作者：梁业由袁伟伟朱杰宁朱文思林秋雄邹笑邓春玉杨敏余细勇单志新 Southern Medical University Guangdong General Hospital Guangdong Provincial Cardiovascular InstituteGuangdong Academy of Medical Sciences

Background Evidences show that macrophage migration inhibitory factor （MIF） and the subtype 4 form of glucose transporter （GLUT4） participate in the process of diabetic cardiomyopathy （DCM）, however the effect of MIF on modulation of GLUT4 expression is not clear. The present study aimed to investigate the mechanism underlying the modulation of GLUT4 by MIF in cardiomyocytes. Methods The neonatal C57BL/ 6 mouse ventricular cardiomyocytes （NMVCs） were isolated for in vitro studies. Expressions of GLUT4 and the candidate GLUT4 regulation associated transcription factors in mouse myocardium and NMVCs were determined by quantitative reverse transcription PCR （qRT-PCR）, and Western blotting, respectively. The effects of screened transcription factors on mediating MIF-promoted GLUT4 expression were verified by RNA interference （RNAi） assay. Results MIF was upregulated, but GLUT4 was decreased in the diabetic myocardium of the db/db mice. MIF could enhance glucose uptake of the cultured neonatal mouse cardiomyocytes with significant upregulation of GLUT4. RT-qPCR and Western-blot assays showed that MEF2A, -2C, -2D and Zacl were significantly up-regulated in MIF-treated NMVCs. Knockdown of Zacl, MEF2A, -2C, and -2D could markedly inhibit glucose uptake and GLUT4 expression in cardiomyocytes. Moreover, Zacl was also shown directly regulated by MEF2A, -2C, and -2D, respectively. Conclusions Transcription factors Zacl and MEF2 mediate MIF-promoted GLUT4 expression in cardiomyocytes.

关键词： macrophage migration inhibitory factor GLUT4 insulin signaling cardiomyocyte diabetes

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Design of Agents Interacting with Immunoregulating Proteins:Potential Inhibitors of the Phenylpyruvate Tautomerase Activity Catalysed by macrophage migration inhibitory factor (MIF)

引用

Chinese Journal of Chemistry 2003年第10期21卷 1256-1262页

作者： CARPY Alain J.M. HAASBROEK P.P. OLIVER D.W. PTC-UMR 5472 CNRS Department of Pharmacy and PharmacologyPharmacology Faculty of Health Science University of Bordeaux ITalence France University of Witwatersrand JohannesburgSouth AfricaPotchefstroom University for CHE PotchefstroomSouth Africa

The macrophage migration inhibitory factor has been implicated in a number ofimmune and inflammatory processes. MIF presents particular opportunities for drug design anddevelopment with potential therapeutic applications. Drug design strategies taking intoconsideration of specific stereochemical and tautomeric requirements in the interaction of MIF withsubstrates and inhibitors allow several novel structures to be designed. Our investigationssuccessfully explored the tautomeric and stereochemical aspects of new compounds of the2-phenylpyruvic acid type, both experimentally, through synthesis and structural investigations andcomputationally, through molecular mechanics and quantum mechanics calculations.

关键词： macrophage migration inhibitory factor phenylpyru-vate tautomerase activity azlactone phenylpyruvic acid derivative

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

macrophage migration inhibitory factor suppresses angiotensinⅡ-induced expression of fibrosis-associated genes by inactivating Smad3 and activating Nrf2 in cardiac fibroblasts

引用

South China Journal of Cardiology 2017年第4期18卷 312-319页

作者：肖珍邹笑朱杰宁梁景南林秋雄邓春玉杨敏符永恒薛玉梅吴书林单志新 Guangdong Cardiovascular Institute Guangdong Provincial Key Laboratory of Clinical Pharmacology Guangdong General Hospital Guangdong Academy of Medical Sciences Shantou University Medical College Shantou University

Background macrophage migration inhibitory factor （MIF） is a key pro-inflammatory cytokine, exhibiting antioxidant properties. However, the role of MIF in cardiac fibrosis is not well known. In the present study, the effects of MIF on Smad3 and Nrf2 signalings in cardiac fibroblasts were investigated. Methods Cardiac fibroblasts were isolated from 1-3 days old C57BL/6 mice, and the cardiac fibroblasts from passage 2 to 4 were used in this study. Expression of fibrosis-associated Collal, Col3al and oL-SMA in mouse cardiac fibroblasts was de- tected by immunofluorescence staining and Western-blot assay, respectively. Intracellular oxidants in mouse car- diac fibroblasts were measured by using the probe dichlorofluoroscindiacetate （DCFH-DA） under confocal mi- croscopy. Western-blot assay was also used to detect Smad3 and Nrf2, antioxidant proteins, MLL and HCF-1 in mouse cardiac fibroblasts. Results Immunofluorescence staining and Western- blot assay showed that MIF could markedly inhibit fibrosis-associated Collal, Col3al and oL-SMA expression in cardiac fibroblasts. DCFH- DA staining revealed that MIF can efficiently decrease reactive oxygen species （ROS） level in Ang-II-induced cardiac fibroblasts. Additionally, Smad3 activation was inhibited, but transcription factor Nrf2 and the downstream antioxidant genes, including HO-1, SOD-l, SOD2, Trx-2 and e-NOS, were increased in MIF-treated cardiac fibroblasts. MLL and HCF-lwere up-regulated by MIF, and either MLL knockdown or HCF-1 knock- down could consistently suppress Nrf2 expression in cardiac fibroblasts. Conclusions MIF possesses anti-fibro- sis effect by inactivating Smad3 and activating Nrf2 in cardiac fibroblasts.

关键词： macrophage migration inhibitory factor cardiac fibrosis Nrf2 Smad3 cardiac fibroblast

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Brain-derived neurotrophic factor mediates macrophage migration inhibitory factor to protect neurons against oxygen-glucose deprivation

引用

Neural Regeneration Research 2020年第8期15卷 1483-1489页

作者： Su Hwan Bae Mi Ran Yoo Ye Yeong Kim In Kyung Hong Mi Hee Kim Seung Hak Lee Dae Yul Kim Department of Rehabilitation Medicine Asan Medical CenterUniversity of Ulsan College of MedicineSeoulRepublic of Korea Asan Institute for Life Sciences Asan Medical CenterUniversity of Ulsan College of MedicineSeoulRepublic of Korea

macrophage migration inhibitory factor(MIF)is a chemokine that plays an essential role in immune system *** studies suggested that MIF protects neurons in ischemic ***,few studies are reported on the role of MIF in neurological recovery after ischemic *** purpose of this study is to identify the molecular mechanism of neuroprotection mediated by *** neuroblastoma cells were incubated in Dulbecco’s modified Eagle’s medium under oxygen-glucose deprivation(OGD)for 4 hours and then returned to normal aerobic environment for reperfusion(OGD/R).30 ng/mL MIF recombinant(30 ng/mL)or ISO-1(MIF antagonist;50μM)was administered to human neuroblastoma *** cell cultures were assigned to one of four groups:control,OGD/R,OGD/R with MIF,OGD/R with *** viability was analyzed using WST-1 *** levels of brain-derived neurotrophic factor(BDNF),microtubule-associated protein 2(MAP2),Caspase-3,Bcl2,and Bax were detected by western blot assay and immunocytochemistry in each group to measure apoptotic ***-1 assay results revealed that compared to the OGD/R group,cell survival rate was significantly higher in the OGD/R with MIF group and lower in the OGD/R with ISO-1 *** blot assay and immunocytochemistry results revealed that expression levels of BDNF,Bcl2,and MAP2 were significantly higher,and expression levels of Caspase-3 and Bax were significantly lower in the MIF group than in the OGD/R *** levels of BDNF,Bcl2,and MAP2 were significantly lower,and expression levels of Caspase-3 and Bax were significantly higher in the ISO-1 group than in the OGD/R *** administration promoted neuronal cell survival and induced high expression levels of BDNF,MAP2,and Bcl2(anti-apoptosis)and low expression levels of Caspase-3 and Bax(pro-apoptosis)in an OGD/R *** results suggest that MIF administration is effective for inducing expression of BDNF and leads to neuroprotection of neuronal cells

关键词： apoptosis brain-derived neurotrophic factor hypoxia in vitro ischemic stroke macrophage migration inhibitory factor nerve regeneration neuroprotective effect reperfusion

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

D-dopachrome tautomerase from Japanese sea bass(Lateolabrax japonicus) is a chemokine-like cytokine and functional homolog of macrophage migration inhibitory factor

引用

Zoological Research 2020年第1期41卷 39-50页

作者： Feng Xu Ming-Yun Li Jiong Chen State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-Products Ningbo UniversityNingboZhejiang 315211China Laboratory of Biochemistry and Molecular Biology School of Marine SciencesNingbo UniversityNingboZhejiang 315832China Key Laboratory of Applied Marine Biotechnology of Ministry of Education Ningbo UniversityNingboZhejiang 315832China

D-dopachrome tautomerase(DDT),a member of the macrophage migration inhibitory factor(MIF)protein superfamily,is a newly described cytokine with chemokine-like ***,research on fish DDT remains *** this study,we identified a DDT homolog(LjDDT)from the Japanese sea bass,Lateolabrax *** analysis showed that LjDDT had typical sequence features of known DDT and MIF homologs and was most closely related to DDT of rock bream(Oplegnathus fasciatus).LjDDT transcripts were detected in all tested tissues of healthy Japanese sea bass,with the highest expression found in the *** infection with Vibrio harveyi,LjDDT transcripts were significantly down-regulated in the three tested tissues,including the liver,spleen,and head *** LjDDT(rLjDDT)and the corresponding antibody(anti-rLjDDT)were subsequently *** administration of 100μg/g anti-rLjDDT had a statistically significant protective effect on the survival of ***-infected ***,rLjDDT was able to induce the migration of monocytes/macrophages(MO/MФ)and lymphocytes both in vitro and in vivo,but without significant influence on the migration of *** exhibited chemotactic activity for lipopolysaccharide(LPS)-stimulated M1-type MO/MΦin vitro,but not for cAMP-stimulated M2-type MO/MΦ.Furthermore,the knockdown of LjCD74,but not LjCXCR4,significantly down-regulated the rLjDDT-enhanced migration of MO/MΦand relieved the rLjMIF-inhibited migration of MO/MΦ.These results indicate that LjCD74 may be the major chemotactic receptor of LjDDT and LjMIF in Japanese sea bass MO/MΦ.Combined rLjDDT+rLjMIF treatment had no significant effect on the migration of MsiRNA,LjCD74si-,or LjCXCR4sitreated MO/MΦcompared to the control group,suggesting that the roles of LjDDT and LjMIF may be *** conclusion,our study demonstrates for the first time that DDT may play a role in the immune responses of fish against bacterial infection through chemotactic

关键词： Cell migration D-dopachrome tautomerase Japanese sea bass macrophage migration inhibitory factor Monocyte/macrophage

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Association of the macrophage migration inhibitory factor promoter polymorphisms with benign lymphoepithelial lesion of lacrimal gland

引用

International Journal of Ophthalmology(English edition) 2017年第8期10卷 1229-1232页

作者： Qin-Jian Li Peng-Xiang Zhao Xu-Juan Zhang Yang Yi Dan-Ying Cheng Jian-Min Ma Xue-Mei Ma College of Life Science and Bio-engineering Beijing Universityof Technology Beijing 100124 China Institute of Infectious Diseases Beijing Ditan HospitalCapital Medical University Beijing 100015 China Beijing Tongren Eye Center Beijing Tongren HospitalCapital Medical University Beijing Ophthalmology &VisionScience Key Lab Beijing 100730 China

AIM： To identify the association of the macrophage migration inhibitory factor （MIF） gene polymorphism with the susceptibility of benign lymphoepithelial lesions （BLEL） of the lacrimal gland. METHODS： A total of 40 BLEL of lacrimal gland cases were matched with 40 healthy subjects （HS）. Extraction the plasma and whole blood DNA of patients of lacrimal gland BLEL and HS. Elisa and polymerase chain reaction was used to determine in plasma contents of MIF and MIF gene SNP-173G〉C and STR -794 CATT（8） polymorphism, respectively. RESULTS： The MIF levels in plasma were significantly higher in patients with lacrimal gland *** versus HS （P〈0.001）. The -173 G〉C MIF polymorphism was significantly associated with lacrimal gland BLEL, with a significantly higher frequency of the C allele in lacrimal gland BLEL patients compared with HS （OR=2.38, 95% C1=1.07-5.31, P=0.032）, and the -173 C/x is more frequent in patients than in HS, P=0.037. Besides, we found that the carriage rate of the MIF -173C/x is associated with higher plasma levels of MIF in the BLEI. of lacrimal gland. CONCLUSION： MIF -173G/C variants play an insidious role in susceptibility of BLEL of lacrimal gland. Otherwise,there is no statistically significant correlation exists between MIF-794 CATT （） and BLEL of lacrimal gland.

关键词： benign lymphoepithelial lesion lacrimal gland macrophage migration inhibitory factor gene polymorphism

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

macrophage migration inhibitory factor promotes breast cancer cell proliferation and metastasis via AMPK pathway

Macrophage migration inhibitory factor promotes breast cance...

引用

2018年中国肿瘤标志物学术大会暨第十二届肿瘤标志物青年科学家论坛

作者： Minjie Wang Yulong Bao Li Wang Lin Shi Fen Yun Xia Liu Yongxia Chen Yongfeng Jia School of Basic Medical Sciences Inner Mongolia Medical University Inner Mongolia Cancer Hospital

Background: macrophage migration inhibitory factor(MIF) is a pleiotropic cytokine with crucial roles in cell proliferation, tumorigenesis, angiogenesis and represents a target gene for therapy in the treatment of breast cancer. AMP-activated protein kinase(AMPK) is a nutrient-andmetabolic stress-sensing enzyme activated by the tumor suppressor kinase. The effect and relationship between MIF and AMPK on breast carcinoma cells is elusive. Our aim is to investigate the effect and mechanism of MIF and AMPK on proliferation and metastasis of breast cancer cells. Methods: MCF-7 breast carcinoma cells were used to investigate effects of MIF and AMPK. MIF levels was determined by Elisa kit. Genetic and protein expression of AMPK, MIF, LKB1 were quantified by quantitative polymerase chain reaction and Western Blotting. Cell proliferation was studied by BrdU *** adhesion by Matrigel adhesion assay, and cell invasion by migration assay through Matrigel-coated filters using the Transwell system. Results: In this study, we demonstrated that under hypoxia microenvironment, MIF levels from MCF-7 breast cancer cells was increased. mRNA expression of MIF was up-regulated as well as the MIF protein expression. MIF up-regulating also results in inhibition of AMPK activity, and the concurrent and phosphorylation of AMPK were decreased under hypoxia conditions. LKB1, upstream gene of AMPK, was also inhibited. Ultimately,MIF up-regulating induced cell proliferation and adhesion of MCF-7 breast carcinoma ***: We conclude that under hypoxia conditions, MIF inhibit AMPK activation, induce proliferation and metastasis on MCF-7 breast carcinoma cells. MIF-AMPK pathway may play a pivotal role in the treatment of breast cancer.

关键词： macrophage migration inhibitory factor AMP-activated protein kinase Breast cancer cell Proliferation Metastasis

来源： cnki会议评论

在线全文

cnki会议

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：