现代预防医学

miR-150-5p经TLR7/NF-κB轴抑制氧化应激与免疫浸润改善糖尿病肾病

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冉娇娇 , 刘婧 , 张晶 , 赵晨旭 , 王楚盈 , 李玉梅

现代预防医学 | 实验技术及其应用 2026,53(2): 339-348

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现代预防医学 |实验技术及其应用 2026 , 53 (2) : 339 -348

miR-150-5p经TLR7/NF-κB轴抑制氧化应激与免疫浸润改善糖尿病肾病

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冉娇娇, 刘婧, 张晶, 赵晨旭, 王楚盈, 李玉梅

作者信息

长春中医药大学药学院，吉林长春 130117

通讯作者:

王楚盈和李玉梅为共同通信作者。

王楚盈，E-mail: wangcy@ccucm.edu.cn

李玉梅，E-mail: liym01@ccucm.edu.cn

作者简介:

冉娇娇（1999—），女，硕士在读，研究方向：中药药性理论及中药作用机制研究

miR-150-5p inhibits oxidative stress and immunological infiltration via the TLR7/NF-κB axis to improve diabetic nephropathy

Jiao-jiao RAN, Jing LIU, Jing ZHANG, Chen-xu ZHAO, Chu-ying WANG, Yu-mei LI

Affiliations

School of Pharmacy, Changchun University of Chinese Medicine, Changchun, Jilin 130117, China

出版时间: 2026-01-25 doi: 10.20043/j.cnki.MPM.202508064

文章导航

摘要

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目的

糖尿病肾病（DN）的发生发展与慢性炎症密切相关，且慢性炎症在氧化应激（OS）和免疫代谢改变间存在复杂的相互作用，共同推动疾病进展。因此，本研究旨在确定DN中OS和免疫相关生物标志物及其潜在治疗靶点。

方法

下载GSE142153，评估其中样本的免疫细胞浸润情况，同时对该数据集进行差异分析，将所得差异基因（DEGs）与OS相关基因（OSRGs）相交以鉴定DN过程中的OS相关差异表达基因（DE-OSRGs）。通过功能富集分析明确DE-OSRGs的生物学作用，构建蛋白互作网络（PPI），结合cytoHubba插件中MCC算法筛选出核心DE-OSRGs，并通过ROC诊断曲线验证其可靠性后，将DE-OSRGs的靶miRNA与DN相关microRNA进行交叉分析后筛选出miR-150-5p。最后通过大鼠DN模型验证核心DE-OSRGs的表达及靶miRNA的作用机制。

结果

生物信息学分析筛选出Toll样受体7（TLR7）为核心DE-OSRGs，并结合靶miRNA预测确定miR-150-5p为研究重点。动物实验表明，miR-150-5p agomir显著下调TLR7和NF-κB p65的表达（P<0.05），减少氧化应激标志物丙二醛（MDA）的生成（P<0.05），并提高超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）的活性（P<0.05）。此外，miR-150-5p还抑制了肿瘤坏死因子α（TNF-α）、白介素-6（IL-6）和白介素-1β（IL-1β）的分泌（P<0.05），减轻免疫细胞浸润，改善肾脏病理损伤。

结论

miR-150-5p通过下调TLR7表达，调控NF-κB信号通路，有效减轻DN中的OS损伤和炎症反应，改善肾脏功能。

关键词

糖尿病肾病 / 氧化应激 / TLR7 / NF-κB / miR-150-5p

Abstract

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Objective

To identify oxidative stress (OS)- and immune-related biomarkers and their therapeutic targets in diabetic nephropathy (DN). The development of DN is closely associated with chronic inflammation, which exhibits complex interactions between OS and immune-metabolic alterations, collectively driving disease progression.

Methods

Download the GSE142153 dataset and evaluate immune cell infiltration in its samples. Simultaneously perform differential analysis on this dataset, intersecting the resulting differentially expressed genes (DEGs) with overall survival-related genes (OSRGs) to identify OS-related differentially expressed genes (DE-OSRGs) in the DN process. Functional enrichment analysis clarified the biological roles of DE-OSRGs. A protein-protein interaction (PPI) network was constructed, and core DE-OSRGs were selected using the MCC algorithm in the cytoHubba plugin. After validating their reliability via ROC diagnostic curves, target miRNAs of DE-OSRGs were cross-analyzed with DN-related microRNAs to identify miR-150-5p, with binding sites subsequently validated. Finally, the expression of core DE-OSRGs and the mechanism of action of their target miRNAs were validated using a rat DN model.

Results

Bioinformatics analysis identified TLR7 as the core DE-OSRG, and combined with target miRNA prediction, miR-150-5p was determined as the primary focus of this study. Animal experiments demonstrated that miR-150-5p agomir significantly downregulated TLR7 and NF-κB p65 expression (P<0.05), reduced the production of malondialdehyde (MDA), a marker of oxidative stress (P<0.05), and increased the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) (P<0.05). Furthermore, miR-150-5p suppressed secretion of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) (P<0.05), mitigated immune cell infiltration, and improved renal pathological damage.

Conclusion

By down-regulating TLR7 and modulating the NF-κB pathway, miR-150-5p attenuates OS injury and inflammation in DN, thereby improving renal function and offering a promising therapeutic target.

Key words

Diabetic nephropathy / Oxidative stress / TLR7 / NF-kB / miR-150-5p

引用本文

冉娇娇, 刘婧, 张晶, 赵晨旭, 王楚盈, 李玉梅. miR-150-5p经TLR7/NF-κB轴抑制氧化应激与免疫浸润改善糖尿病肾病. 现代预防医学, 2026 , 53 (2) : 339 -348 . DOI: 10.20043/j.cnki.MPM.202508064

Jiao-jiao RAN, Jing LIU, Jing ZHANG, Chen-xu ZHAO, Chu-ying WANG, Yu-mei LI. miR-150-5p inhibits oxidative stress and immunological infiltration via the TLR7/NF-κB axis to improve diabetic nephropathy[J]. Modern Preventive Medicine, 2026 , 53 (2) : 339 -348 . DOI: 10.20043/j.cnki.MPM.202508064

正文

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糖尿病肾病（Diabetic Nephropathy，DN）是糖尿病引起的肾脏微血管并发症，以持续性蛋白尿和/或肾小球滤过率逐渐降低为主要临床表现主^[1]。氧化应激（Oxidative Stress，OS）被认为是DN发病的关键因素，高血糖增加了自由基的产生，氧化剂和抗氧化剂水平之间的失衡，从而导致OS^[2-3]。OS可刺激信号分子如核因子-κB（Nuclear Factor-κB，NF-κB）或激活蛋白-1（Activator Protein-1，AP-1）^[4]，诱导肾细胞炎症、凋亡及纤维化；随之释放的趋化因子引起肾脏部位免疫细胞浸润，即外周免疫细胞迁移至肾脏并活化，是DN炎症损伤的关键环节，可致单核-巨噬细胞过度激活，机体免疫稳态失衡^[5-6]。尽管目前针对OS和免疫浸润的治疗策略（如抗氧化剂和抗炎药物）在实验研究中取得了一定进展，但其临床转化仍面临诸多挑战。因此，探索新的治疗靶点和策略以更有效地减轻OS和免疫浸润是DN研究的重要方向。基于生物信息学的研究发现，与OS相关的基因在慢性肾病患者的预后方面具有临床价值^[7]，但目前仍然缺乏对DN和OS的全面和深入的研究。MicroRNA（miRNA）在人体内的变化与病理状况有关，在许多人类疾病中发挥关键作用，是医学研究中的重要介质^[8-9]。miRNA参与各种生物过程的调节，包括先天免疫反应^[10]、适应性免疫反应^[11]和炎症^[12]的调节，并且在DN中与OS存在密切关联，但具体机制尚未完全阐明。本研究运用生物信息学系统解析DN中miRNA与OS相关信号通路的相互作用，并通过动物实验对其关键节点进行功能验证。

1　材料与方法

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1.1　基因的表达数据来源

从美国国家生物技术信息中心（national center of biotechnology information，NCBI）数据库^[13]（http://www.ncbi.nlm.nih.gov/geo）中获取DN相关基因表达微阵列，数据来自GPL571平台的GSE142153（DN=23，CON=10）^[14]。GSE142153基于肾穿刺组织，能直接反映肾脏局部分子改变。利用GENEcards数据库^[15]（https://www.genecards.org/）搜索OS相关基因用于后续分析。

1.2　基因表达数据处理和差异基因表达分析

使用GEO2R在线工具（https://www.ncbi.nlm.nih.gov/geo/geo2r）进行差异表达分析，筛选出满足P<0.05且|log₂FC|>1的差异表达基因（differentially expressed genes，DEGs），与OS相关基因（oxidative stress-related genes，OSRGs）进行交叉分析得到与OS相关的差异表达基因（differentially expressed oxidative stress-related genes，DE-OSRGs）。使用DAVID在线工具（http://www.david.ncifcrf.gov）进行基因本体论^[16]（gene ontology，GO）功能注释和京都基因与基因组百科全书^[7]（Kyotoencyclopedia of genes and genome，KEGG）进行通路分析，以P<0.05为选取标准。

1.3　免疫浸润分析

基于CIBERSORT（CIBERSORT.R脚本分析）核心算法^[18]，利用CIBERSORTx网站（https://cibersortx.stanford.edu）提供的22种免疫细胞的markers来分析GSE142153中各样本的免疫细胞浸润情况。

1.4　核心DE-OSRGs筛选及ROC曲线的绘制

使用STRING数据库^[19]（http://www.string-db.org）构建蛋白质-蛋白质相互作用（protein-protein interaction，PPI）网络，通过Cytoscape软件（version 3.9.1）进行可视化分析，并利用其内置cytoHubba插件的MCC算法鉴定重要的基因簇，获得枢纽基因。基于R软件（4.0.2版本）pROC和ggplot2包，绘制受试者特征曲线（Receiver Operating Characteristic Curve，ROC），以评估获取的核心DE-OSRGs在DN诊断中的敏感性与特异性。计算曲线下面积（Area Under the Curve，AUC）以判定其真实性和可靠性。

1.5　核心DE-OSRGs的microRNA靶点预测

利用RNADisease（http://www.rnadisease.org）数据库^[20]输入关键词“diabetic nephropathy”筛选出符合“Homo sapiens，Score>0.9”的DN相关miRNA，与利用TatgetScan（https://www.targetscan.org）数据库^[21]筛选出DE-OSRGs的靶miRNA进行交叉分析，并查询它们与目标基因的结合位点。

1.6　糖尿病肾病大鼠模型的建立与干预

动物来源于长春市亿斯实验动物技术有限责任公司，经长春中医药大学动物伦理委员会批准（伦理批号：2021161，动物使用许可证号：SCXK（吉）2020-0002）。选用4～5周龄SPF/VAF级雄性SD大鼠（初始体重80～100 g），所有大鼠均饲养于12 h光照/12 h黑暗循环、温度23℃±2℃、相对湿度55%±5%环境中，自由进食饮水。适应性喂养1周后，将大鼠分为对照组（Control组，n=6）与待造模组（n=18）：Control组全程维持普通饲料喂养，同期注射生理盐水；待造模组先给予35%脂肪比高脂饲料喂养6周，再禁食12 h后腹腔注射链脲佐菌素（STZ，50 mg/kg）建立糖尿病模型^[22]，72 h后空腹血糖≥16.7 mmol/L判定成模，继续高脂饲料喂养8周诱导DN模型；高脂饲料和STZ均购自北京博爱港。DN模型成功后，将DN模型大鼠随机分为DN组、miR-150-5p激动剂（miR-150-5p agomir）组、阴性对照（agomir NC）组，每组n=6。后两组分别尾静脉注射miR-150-5p agomir、MicroRNA Agomir Negative Control，剂量均为50 nmol/kg，每周2次，持续4周^[23]；试剂均购自广东锐博。DN组与Control组同期尾静脉注射等量生理盐水。干预期间各组保持原饲料不变，于agomir干预0周（DN成模即刻、尚未给药）及agomir干预5周（末次给药后1周、处死前）通过代谢笼收集24 h尿液；随后处死所有大鼠，腹主动脉采集血液，并剥离双侧肾脏组织。

1.7　生化检测

收集大鼠24 h尿液，采用南京建成和Abcam的试剂盒分别检测尿蛋白排泄率（urinary protein excretion rate，UP）及尿白蛋白/肌酐比值（albumin/creatinine ratio，ACR）。大鼠经麻醉后通过腹主动脉采集血液，采用Crystal Chem的试剂盒检测血清糖化血红蛋白（glycated hemoglobin A1c，HbA1c）水平。同时，检测血清肌酐（serum creatinine，Scr）和尿素氮（blood urea nitrogen，BUN）水平，所用试剂盒均购自南京建成。通过ELISA法进一步检测血清中炎症因子与氧化应激标志物水平：炎症因子包括大鼠肿瘤坏死因子α（tumor necrosis factor-alpha，TNF-α）、白介素-6（interleukin-6，IL-6）和白介素-1β（interleukin-1β，IL-1β），所用试剂盒均购自MeiMian；氧化应激标志物包括超氧化物歧化酶（superoxide dismutase，SOD）、丙二醛（malondialdehyde，MDA）和谷胱甘肽过氧化物酶（glutathione peroxidase，GSH-Px）的活性，其中SOD检测试剂盒购自MeiMian，MDA与GSH-Px检测试剂盒均购自mlbio。

1.8　病理染色和免疫组化

肾脏组织经4%多聚甲醛固定、石蜡包埋，制备4 μm厚切片。取每组1只动物的肾脏切片，经苏木精-伊红（Hematoxylin-Eosin staining，H&E）染色评估组织结构与质量，Masson三色染色检测胶原纤维沉积。H&E染色切片采用盲法由2名病理医师独立进行半定量分析，肾小球硬化按无硬化、部分硬化、完全硬化分别计0、1、2分，并计算每视野平均得分；肾小管间质纤维化按面积<10%、10%～30%、30%～50%、>50%分别计0、1、2、3分^[24]。通过免疫组化染色检测肾脏组织中单核/巨噬细胞标志物CD68（cluster of differentiation 68）、核因子κB p65亚基（nuclear factor kappa B p65 subunit，NF-κB p65）和磷酸化核因子κB抑制蛋白α（phosphorylated inhibitor of nuclear factor kappa B alpha，p-IKBα）的表达。切片经脱蜡、水化后，在柠檬酸/柠檬酸钠缓冲液（pH 6.0）中进行抗原修复，并封闭内源性过氧化物酶；一抗孵育过夜后，再使用二抗孵育，最后进行染色。所用抗体均购自武汉三鹰生物技术有限公司。

1.9　蛋白印迹法和实时荧光定量PCR

组织裂解后，使用Beyotime的BCA蛋白浓度测定试剂盒测定提取的组织蛋白浓度。将等量的蛋白分离后转移到Servicebio的聚偏二氟乙烯（PVDF）膜上，在快速封闭液中封闭15 min。洗涤后一抗孵育过夜，再与辣根过氧化物酶（Horseradish Peroxidase，HRP）偶联的二抗孵育1 h，检测后定量免疫印迹密度。甘油醛-3-磷酸脱氢酶（Glyceraldehyde-3-phosphate dehydrogenase，GAPDH）用作对照，检测肾脏组织中Toll样受体7（Toll-like receptor 7，TLR7）、NF-κB p65、TNF-α、IL-6和IL-1β表达水平，所用抗体均购自武汉三鹰生物技术有限公司。

使用YEASEND的MolPure^® Cell/Tissue miRNA Kit试剂盒从组织中分离总RNA，通过Thermo超微量分光光度计定量后，采用YEASEND的Hifair^® Ⅲ 1st Strand cDNA Synthesis Kit (gDNA digester plus)试剂盒在Eppendorf PCR仪中逆转录等量的RNA样品，最后在Bio-Rad CFX Manager系统上进行qPCR检测，并使用2^-ΔΔCT法分析mRNA和miRNA的相对表达。qPCR检测过程中分别以U6小核RNA（U6 small nuclear RNA，U6）和GAPDH作为上样对照，检测组织或细胞中miR-150-5p和TLR7 mRNA的表达水平。所使用的引物均由生工生物工程有限公司设计和生产。

1.10　实验数据分析方法

使用SPSS 23.0软件进行数据处理与分析。符合正态分布的用均值±标准差（

）表示，方差齐时，多组间比较使用单因素方差分析，进一步两两比较采用LSD进行分析；方差不齐则采用Welch ANOVA，2组比较采用Dunnett T3进行分析。以检验水准α=0.05为差异有统计学意义。

2　结果

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2.1　DEGs的识别及DEOSGs富集函数分析

如图1A-C所示，GSE142153进行差异基因分析后获得200个DEG（86个上调，114个下调），并通过GENEcards数据库筛选Relevance score>3的蛋白编码OSRGs 331 1个，两者相交得到52个DE-OSRG。GO和KEGG分析如图1D-E所示，结果显示GSE142153主要参与细胞因子介导的信号通路，如NF-κB信号通路。其中，Toll样受体（Toll-Like Receptor，TLR）信号通路是NF-κB信号通路的上游。

2.2　核心DE-OSRGs的鉴定和ROC诊断

PPI网络（minimum required interaction score为0.700）如图2A所示，获得前20个关键基因，包含TLR7等7种功能性蛋白，其余13个基因为炎症因子或趋化因子。考察7种功能性蛋白在DN中的表达情况（图2B），并探究它们之间的功能相关性（图2C）。最后通过ROC曲线，如图3A-G可知每个基因的AUC值均在0.7以上，说明特征基因对DN具有较强的预测能力。

2.3　免疫细胞浸润分析

基于GSE142153，通过CIBERSORT算法量化22种免疫细胞在DN与正常肾脏组织中的比例（图4A）。有4种免疫细胞存在显著差异（P<0.05），其中，γδT细胞（gamma delta T cells，γδT cells）和单核细胞（Monocytes）在两组间存在显著差异，且在DN肾脏组织中，树突状细胞（Dendritic cells）及自然杀伤细胞（natural killer cells，NK cells）被激活（图4B）。在此基础上，进一步考察了7种核心DE-OSRG在差异免疫细胞中的相关性（图4C）。

2.4　DE-OSRGs的microRNA靶点预测

将81个DN相关miRNA与556个TLR7靶miRNA进行交叉分析，筛选出21种miRNA（图5A），并验证TLR7与miR-150-5p的结合位点（图5B）。

2.5　DN大鼠尿液和血液中氧化应激标志物的变化

图6~7所示：DN大鼠基础ACR、UP、BUN、Scr及血清MDA、TNF-α、IL-6、IL-1β均显著高于Control组，GSH-Px、SOD活性明显降低（P<0.05）；miR-150-5p agomir干预后，上述肾功能与氧化应激指标均恢复至接近Control水平（P<0.05），而阴性对照组与DN组差异无统计学意义（P>0.05）。值得注意的是，DN组与miR-150-5p agomir组之间HbA1c水平无显著差异（图6C），提示miR-150-5p agomir对血糖控制无直接影响，其肾保护作用主要通过减轻OS和抑制炎症反应实现。

2.6　DN大鼠肾组织中TLR7/NF-κB通路相关蛋白的表达和miR-150-5p的干预

H&E染色结果显示（图8B），与DN组大鼠相比，miR-150-5p agomir组大鼠表现出较少的小管扩张，miR-150-5p干预显著改善了肾小球硬化和肾小管间质纤维化（P<0.05）。Masson染色结果显示（图8C），miR-150-5p agomir组肾脏的纤维化区域比DN组肾脏少，而转染miR-NC后，水平与DN组相比无显著差异。如图9A-E所示，炎症导致免疫浸润相关蛋白CD68在DN大鼠肾脏中的表达显著高于miR-150-5p agomir组大鼠，过表达miR-150-5p显著降低了DN大鼠肾脏中TLR7和NF-κB通路相关蛋白NF-κB p65和p-IκBα的阳性面积（P<0.05）。

2.7　miR-150-5p改善TLR7/NF-κB通路激活所导致的DN大鼠肾脏炎症因子过表达

如图10A所示，在DN组大鼠肾脏组织中，炎症因子和TLR7/NF-κB p65通路蛋白表达跟Control组相比均有所增加（P<0.05）；跟DN组相比，miR-50-5p agomir组NF-κB p65蛋白表达减少，炎症相关蛋白TNF-α、IL-6和IL-1β的表达也降低，炎症有所改善（P<0.05），而agomir NC组水平均与DN组相比无显著差异（P>0.05）。实时荧光定量PCR结果显示，miR-150-5p agomir组TLR7 mRNA表达较DN组的低（P<0.05），表明miR-150-5p可能通过直接靶向TLR7的3’非翻译区（3’UTR）抑制其表达（图10C）。

3　讨论

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在DN中，OS可激活炎症信号通路导致肾损伤，炎症因子进而促进免疫反应，形成正负反馈进加剧肾损伤。但目前鲜有研究关注DN与正常组织中，与免疫浸润及OS相关的异常表达基因标志物。本研究基于Cibersort算法分析GSE142153中22种免疫细胞浸润情况，结果表明炎症反应的增强，可能通过分泌促炎或抗炎细胞因子影响炎症反应的强度和持续时间。GO/KEGG分析发现，DE-OSRGs主要富集于TLR及NF-κB信号通路，提示炎症相关通路在DN的病理进展中起关键作用。进一步分析通路层级关系可见，TLR信号通路处于上游，其核心基因TLR7介导的炎症反应中，NF-κB信号通路扮演核心角色——其持续激活可诱导促炎细胞因子大量生成，形成“炎症-损伤”正反馈环路，加剧DN肾脏病理损伤。因此，本研究将TLR7与NF-κB信号通路间的调控关联作为核心，并开展后续研究。

TLR信号通路在识别和响应损伤信号方面发挥着重要作用，TLR7是先天免疫系统中的重要模式识别受体^[25]，主要识别单链RNA（single-stranded ribonucleic acid，ssRNA）并介导炎症反应。在DN中，OS诱导的损伤相关分子模式（damage associated molecular patterns，DAMPs）和病原体相关分子模式（Pathogen-associated molecular patterns，PAMPs）可激活TLR7，DAMPs和PAMPs与TLR7结合后，通过髓样分化因子88（myeloid differentiation factor 88，MyD88）和肿瘤坏死因子受体相关因子6（tumor necrosis factor receptor-associated factor 6，TRAF6）等分子传递信号^[26-27]，导致核因子κB抑制蛋白α（inhibitor of nuclear factor kappa B alpha，IκBα）的磷酸化和降解，从而释放NF-κB（p65/p50），使其能够转移到细胞核结合DNA的特定序列，调控基因转录^[28]。NF-κB在细胞核中结合到多种促炎基因的启动子区域，促进IL-6、TNF-α、IL-1β等促炎细胞因子的表达，同时激活其他炎症相关分子，如环氧化酶-2（cyclooxygenase-2，COX-2）、诱导型一氧化氮合酶（inducible nitric oxide synthase，iNOS），加剧OS和炎症反应，进一步加重糖尿病肾病的病理损伤^[29-30]。因此，TLR7/NF-κB信号通路在糖尿病肾病的OS和免疫浸润中扮演了关键角色。

有研究表明^[31-32]，miR-150-5p在脓毒症诱导的急性肾损伤中发挥保护作用，上调miR-150-5p可减轻了肾脏炎症反应和OS。在慢性肾病中，miR-150-5p减轻OS缓解肾损伤的作用日益得到关注，但TLR7与miR-150-5p之间的关系目前尚不明确。因此，本文聚焦TLR7/miR-150-5p轴，并进行动物实验验证。结果表明，过表达miR-150-5p显著下调TLR7和NF-κB p65的表达，减少OS标志物（如MDA）的生成，并提高抗氧化酶（如SOD、GSH-Px）的活性。此外，miR-150-5p还抑制了炎症因子（如TNF-α、IL-6）的分泌，减轻了免疫细胞浸润，改善了肾脏病理损伤。这表明miR-150-5p可通过下调TLR7的表达调控NF-κB信号通路从而有效减轻了DN中的OS损伤和炎症反应，改善了肾脏功能。

本研究首次通过生物信息学分析与实验验证，揭示miR-150-5p可直接靶向TLR7的3’UTR抑制其表达，阻断NF-κB信号通路激活，减轻DN中OS与免疫浸润，为DN治疗提供新潜在靶点，具临床应用前景。研究仍有局限：仅用雄性大鼠，未探索性别差异影响；未验证人类DN肾组织中miR-150-5p/TLR7的表达模式，结论临床适用性需进一步验证。

基金

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吉林省自然科学基金(YDZJ202401005ZYTS)

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2026年第53卷第2期

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doi: 10.20043/j.cnki.MPM.202508064

接收时间：2025-08-05
首发时间：2026-11-02
出版时间：2026-01-25

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收稿日期：2025-08-05

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吉林省自然科学基金(YDZJ202401005ZYTS)

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长春中医药大学药学院，吉林长春 130117

通讯作者:

王楚盈和李玉梅为共同通信作者。

王楚盈，E-mail: wangcy@ccucm.edu.cn

李玉梅，E-mail: liym01@ccucm.edu.cn

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2种不同金属材料的力学参数

科 Family	属数 Number of genus	种数 Number of species	占总种数比例 Percentage of total species (%)	属 Genus	种数 Number of species	占总种数比例 Percentage of total species (%)
鹅膏菌科Amanitaceae	2	11	5.26	鹅膏菌属 Amanita	10	4.78
小菇科 Mycenaceae	2	12	5.74	丝盖伞属 Inocybe	5	2.39
多孔菌科 Polyporaceae	8	14	6.70	蜡蘑属 Laccaria	5	2.39
红菇科 Russulaceae	3	23	11.00	小皮伞属 Marasmius	6	2.87
				小菇属 Mycena	11	5.26
				光柄菇属 Pluteus	5	2.39
				红菇属 Russula	17	8.13
				栓菌属 Trametes	5	2.39

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