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李琼;张沙沙 《中国细胞生物学学报》2025,(8):1909-1917
该文旨在探讨槲皮素(Que)对荨麻疹(urticaria)大鼠免疫炎症反应及Janus激酶2/信号转导与转录激活子3(JAK2/STAT3)信号通路的影响。建立荨麻疹大鼠模型,将所有实验大鼠分为对照组(Control组)、模型组(Urticaria组)、槲皮素低剂量组(Que-L组)、槲皮素高剂量组(Que-H组)、槲皮素高剂量+JAK2/STAT3信号通路激活剂组(Que-H+Colivelin组);直尺测量大鼠皮肤蓝斑直径;流式细胞术检测Th1、Th2水平; ELISA法检测血清炎症因子白细胞介素-4(IL-4)、γ干扰素(IFN-γ)水平及血清免疫指标IgE水平;甲苯胺蓝染色法观察皮肤肥大细胞脱颗粒变化; HE染色观察皮肤病理变化;免疫印迹法检测JAK2、p-JAK2、STAT3、p-STAT3表达水平。Urticaria组较Control组皮肤细胞结构紊乱,细胞间隙增宽,可见大量炎症细胞浸润,肥大细胞明显增多,脱颗粒现象加重,组织水肿明显,背部皮肤蓝斑直径增大, Th1淋巴细胞比例及IFN-γ水平降低, Th2淋巴细胞比例, IL-4、IgE水平及p-JAK2/JAK2、p-STAT3/STAT3表达水平升高(P<0.05); Que-L、Que-H组较Urticaria组皮肤细胞结构依次排列相对整齐,细胞间隙增宽及炎症细胞浸润依次减轻,肥大细胞明显减少,脱颗粒现象减轻,背部皮肤蓝斑直径依次减小, Th1淋巴细胞比例及IFN-γ水平升高,Th2淋巴细胞比例, IL-4、IgE水平及p-JAK2/JAK2、p-STAT3/STAT3表达水平降低(P<0.05); QueH+Colivelin组较Que-H组皮肤细胞结构紊乱加重,细胞间隙增宽及炎症细胞浸润增多,肥大细胞明显增多,脱颗粒现象加重,组织水肿明显,背部皮肤蓝斑直径增大, Th1淋巴细胞比例及IFN-γ水平降低, Th2淋巴细胞比例, IL-4、IgE水平及p-JAK2/JAK2、p-STAT3/STAT3表达水平升高(P<0.05)。槲皮素可减轻荨麻疹大鼠免疫炎症反应,其机制与抑制JAK2/STAT3信号通路有关。 相似文献
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目的：探讨Janus激酶2-信号转导子和转录激活子3（JAK2/STAT3）信号通路在运动预适应（EP）抗心肌细胞凋亡中的作用及其机制。方法：健康雄性SD大鼠80只,随机分为对照组（C组）、力竭组（EE组）、运动预适应组（EP组）、运动预适应+AG490组（EP+AG组）（n=20）。连续3 d的间歇跑台运动建立EP动物模型,力竭运动致大鼠运动性心肌损伤。采用TUNEL法检测心肌细胞凋亡改变、Western blot法检测心脏Caspase-3定量表达的变化,免疫组织化学法和Western blot法显示心脏p-JAK2和p-STAT3定位和定量表达的变化。结果：与C组相比,EE组心肌细胞凋亡、心脏Caspase-3、p-JAK2和p-STAT3的表达均显著升高;与EE组相比,EP组心肌细胞凋亡和心脏Caspase-3表达明显降低,而心脏p-JAK2和p-STAT3表达显著升高;与EP组相比,EP+AG组心肌细胞凋亡和心脏Caspase-3表达均显著升高,而心脏p-JAK2和p-STAT3表达明显降低。结论：EP可诱导心脏磷酸化JAK2和STAT3表达增加,减少心脏Caspase-3的表达,抑制心肌细胞凋亡,提示JAK2/STAT3信号通路参与了EP抗心肌细胞凋亡的作用。 相似文献
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赵东利;李竹茜 《中国细胞生物学学报》2025,(8):1939-1947
该文旨在探究芹菜素对痤疮模型大鼠Janus激酶2(JAK2)/转录激活因子3(STAT3)信号通路、炎症反应及凋亡的影响。将60只大鼠随机分为空白对照组、模型组、低剂量(L)-芹菜素组、高剂量(H)-芹菜素组和H-芹菜素+JAK2激活剂Coumermycin A1组,每组12只。除空白对照组外,其余组大鼠均采用痤疮丙酸杆菌构建痤疮模型。酶联免疫吸附实验(ELISA)检测大鼠血清中白介素-1β(IL-1β)、IL-8、IL-6、肿瘤坏死因子-α(TNF-α)表达情况;苏木素伊红(HE)染色观察右耳皮肤组织变化; TUNEL染色观察右耳皮肤组织细胞凋亡; qRT-PCR检测凋亡调控基因B淋巴细胞瘤-2(Bcl-2)和胱天蛋白酶3(Caspase-3)的mRNA表达情况; Western blot检测Bcl-2、Caspase-3、裂解的胱天蛋白酶3(Cleaved Caspase-3)及JAK2/STAT3通路相关蛋白表达情况。结果显示,与空白对照组比较,模型组大鼠右耳厚度增加、皮肤肿胀、细胞凋亡增加,血清中IL-8、IL-1β、IL-6、TNF-α水平升高, Caspase-3 mRNA表达水平及Cleaved Caspase-3/Caspase-3水平升高, Bcl-2 mRNA和蛋白表达水平降低, p-JAK2/JAK2和p-STAT3/STAT3值升高(P<0.05);与模型组比较, L-芹菜素组和H-芹菜素组大鼠右耳厚度变薄、皮肤肿胀减轻、细胞凋亡减少,血清中IL-8、IL-1β、IL-6、TNF-α水平降低, Caspase-3 mRNA表达水平及Cleaved Caspase-3/Caspase-3水平降低, Bcl-2 mRNA和蛋白表达水平升高, p-JAK2/JAK2和p-STAT3/STAT3值降低(P<0.05),且H-芹菜素组变化优于L-芹菜素组(P<0.05);与H-芹菜素组比较, H-芹菜素+Coumermycin A1组大鼠p-JAK2/JAK2和pSTAT3/STAT3值升高,右耳皮肤痤疮症状和炎症反应加重。总之,芹菜素可能通过抑制JAK2/STAT3信号通路抑制痤疮模型大鼠炎症反应。 相似文献
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基于IL-6/JAK2/STAT3信号通路探讨岩白菜素对四氯化碳(CCl4)致大鼠急性肝损伤的保肝作用及其作用机制.60只SD大鼠随机分为正常组、模型组、水飞蓟素(120 mg/kg)组、岩白菜素低、中、高(20、40、80 mg/kg)剂量组,每组10只.水飞蓟素组、岩白菜素各剂量组大鼠按照10 mL/kg灌胃给药,... 相似文献
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目的:探讨Janus蛋白酪氨酸激酶2/信号转导子和转录激活子3(JAK2/STAT3)信号通路在门静脉高压大鼠模型脾脏纤维化过程中的表达和作用.方法:采用缩窄门静脉的方法制备门静脉高压大鼠模型,通过给予JAK2特异性抑制剂AG490阻断JAK2/STAT3信号通路.30只SD(Sprague Dawley)大鼠随机分为单纯手术组、AG490组、假手术组(n=10).AG490组每天给予5 mg/kg体重的AG490,另外两组每天给予相同体积的生理盐水,连续2周后处死大鼠,计算各组脾指数,Masson三色染色检测脾脏组织纤维化程度,免疫组织化学和Western blotting检测脾脏组织中磷酸化STAT3 (p-STAT3)蛋白的表达水平.结果:单纯手术组p-STAT3蛋白水平较假手术组明显升高(P＜0.05),AG490组较单纯手术组明显降低(P＜0.05);单纯手术组脾指数、脾脏纤维化程度较假手术组明显升高(P＜0.05),AG490组较单纯手术组明显降低(P＜0.05);p-STAT3蛋白水平与脾脏纤维化程度呈明显的正相关趋势(r=0.897,P＜0.05).结论:JAK2/STAT3信号通路与门静脉高压大鼠脾脏纤维化过程关系密切,阻断该通路可以减轻门静脉高压脾脏纤维化的程度. 相似文献
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冯自力;陈映茹;赵鹏;陈美君;周良弘;杨珏;郝小江 《天然产物研究与开发》2025,(12):2194-2204+2273
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摘要 目的：探讨LncRNA-NEAT1对妊娠期高血压大鼠JAK2/STAT3信号通路、炎症反应和妊娠结局的影响。方法：采用注射L-精氨酸甲酯的方法构建妊娠期高血压大鼠模型。采用Western blot检测JAK2/STAT3信号通路蛋白表达;采用ELISA法检测炎症因子和血管内皮损伤因子。观察并记录大鼠24 h蛋白尿、尾静脉压和死胎率。结果：与空白组相比,模型组、LncRNA-NEAT1过表达组、LncRNA-NEAT1抑制组JAK2、STAT3的蛋白表达水平明显更高（P＜0.05）;与模型组相比,LncRNA-NEAT1抑制组JAK2、STAT3的蛋白表达水平明显更低（P＜0.05）,而LncRNA-NEAT1过表达组JAK2、STAT3的蛋白表达水平明显更高（P＜0.05）;与空白组相比,模型组、LncRNA-NEAT1过表达组、LncRNA-NEAT1抑制组ET-1和sICAM-1水平明显更高,而NO水平明显更低（P＜0.05）;与模型组相比,LncRNA-NEAT1过表达组、LncRNA-NEAT1抑制组ET-1和sICAM-1水平明显更高（P＜0.05）,而NO水平明显更低（P＜0.05）,而LncRNA-NEAT1过表达组ET-1和sICAM-1表达水平明显更高,而NO明显更低（P＜0.05）;与空白组相比,模型组、LncRNA-NEAT1过表达组、LncRNA-NEAT1抑制组TNF-α、IL-1β、IL-18表达水平明显更高（P＜0.05）;与模型组相比,LncRNA-NEAT1抑制组TNF-α、IL-1β、IL-18表达水平明显更低（P＜0.05）,而LncRNA-NEAT1过表达组TNF-α、IL-1β、IL-18表达水平明显更高（P＜0.05）;与空白组相比,模型组、LncRNA-NEAT1过表达组、LncRNA-NEAT1抑制组尾静脉压和24h蛋白尿水平明显更高（P＜0.05）;与模型组相比,LncRNA-NEAT1抑制组尾静脉压和24 h蛋白尿表达水平明显更低（P＜0.05）,而LncRNA-NEAT1过表达组尾静脉压和24 h蛋白尿表达水平明显更高（P＜0.05）;LncRNA-NEAT1过表达组（21.56%）死胎率显著高于模型组（16.72%）和LncRNA-NEAT1抑制组（5.65%）。结论：妊娠期糖尿病大鼠LncRNA-NEAT1的表达下调可抑制JAK2/STAT3信号通路的表达并下调下游促炎因子的表达,进而缓解血管内皮损伤降低死胎率。 相似文献
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Chunqiu Xiong Bingbing Yan Suhua Xia Fei Yu Jingjing Zhao Hua Bai 《Saudi Journal of Biological Sciences》2021,28(9):4900-4907
Ovarian cancer is one of the deadliest gynecologic malignancies and is the seventh leading cause of mortalities and morbidities globally. Although there are various therapeutic strategies, a major challenge for scientific community is to come up with effective strategy to treat ovarian cancer. Tilianin, a polyphenol flavonoid is well known for its extensive biological actions like cardioprotective, neuroprotective, anti-oxidant, anti-inflammatory, anti-diabetic and anti-tumor properties. The current study is designed to investigate the anti-cancer action of Tilianin in ovarian cancer (PA-1) cells. The findings of this study revealed that Tilianin treatment results in significant and concentration dependent decrease in cell viability. The growth inhibiting action of Tilianin is associated with apoptosis which was confirmed by DAPI and AO/EtBr staining. The Tilianin-triggered apoptosis in PA-1 cells was correlated with elevated generation of ROS, loss of mitochondrial membrane potential, alterations in pro-apoptotic (upregulated mRNA expression of Bax) and anti-apoptotic (downregulated mRNA expression of Bcl2) factors and activation of caspase-8, −9 and −3. Cell cycle analysis revealed that Tilianin treatment prevented G1/S transition through reduced mRNA expression of cyclin D1. Additionally, the findings of this study also showed Tilianin inhibited JAK2/STAT3 signaling (downregulated expression of pJAK2, JAK2, pSTAT3, and STAT3) with no change in mRNA expression level of ERK indicating its non-involvement in the apoptotic and/or growth inhibition of ovarian cancer cells. In conclusion, the findings of this exploration provided clear evidence of anti-cancer effects of Tilianin in PA-1 cells through its anti-proliferative action, ability to induce apoptosis both through extrinsic and intrinsic pathways, cell cycle (G1/S) arrest and JAK2/STAT3 signaling inhibition. 相似文献
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Suresh Mickymaray Faiz Abdulaziz Alfaiz Anand Paramasivam Vishnu Priya Veeraraghavan Nanthini Devi Periadurai Krishna Mohan Surapaneni Guangfeng Niu 《Saudi Journal of Biological Sciences》2021,28(7):3641-3649
Osteosarcoma is the frequent pediatric bone cancer where pediatric osteosarcoma incidences are more than 10% within the population. Most of the patients with osteosarcoma fall within the age of 15–30 years. Therefore, in this research, we examined the anticancer effect of Rhaponticin against the human osteosarcoma (MG-63) cells. The cytotoxicity of Rhaponticin on the MC3T3-E1 and MG-63 cells was examined through the MTT assay. The intracellular ROS accumulation, cell nuclear morphological alterations, apoptotic cell death and nuclear damages, and MMP status of Rhaponticin administered MG-63 cells were inspected by fluorescent staining techniques. The cell migration was assessed through scratch assay. The mRNA expressions of PI3K-Akt-mTOR signaling proteins were studied by RT-PCR analysis. Rhaponticin showed potent cytotoxicity, substantially inhibited the MG-63 cell growth, and displayed morphological alterations. However, rhaponticin did not affect the MC3T3-E1 cell viability. Rhaponticin administered MG-63 cells demonstrated augmented intracellular ROS accretion, weakened MMP, increased nuclear damages, and increased apoptosis. Rhaponticin effectively down-regulated the PI3K-Akt-mTOR signaling cascade in the MG-63 cells. These outcomes proved that the Rhaponticin can be a hopeful chemotherapeutic agent in the future to treat human osteosarcoma. 相似文献
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目的:研究不同浓度白花丹素对骨肉瘤细胞MG-63凋亡迁移、基质金属蛋白酶(MMP)及Bcl-2、Bax、Ezrin蛋白表达的影响。方法:取对数生长期的骨肉瘤MG-63细胞,传代培养成细胞株后以随机法分成对照组、低剂量组、中剂量组、高剂量组。其中对照组加入到0.1%浓度的DMSO完全培养基中培养,低剂量组、中剂量组、高剂量组分别加入到浓度为5、10、20μmol/L的白花丹素的有关培养基中培养。培养24 h后,采用Transwell法检测MG-63细胞迁移率、Hoechst33342染色法检测MG-63细胞凋亡率、Western blot法检测四组MG-63细胞的MMP-2、MMP-9、Bcl-2、Bax、Ezrin蛋白表达水平。结果:培养24 h后,低剂量组、中剂量组、高剂量组的骨肉瘤细胞MG-63凋亡率及Bax蛋白表达水平均较对照组升高(P<0.05),且随白花丹素浓度的增加而升高(P<0.05);骨肉瘤细胞MG-63的细胞迁移率、MMP-2、MMP-9、Bcl-2及Ezrin蛋白表达水平较对照组降低(P<0.05),且随白花丹素浓度的增加而降低(P<0.05)。结论:白花丹素对骨肉瘤细胞MG-63凋亡的促进作用以及迁移的抑制作用明显,其作用机制可能与抑制骨肉瘤细胞MG-63中的MMP-2、MMP-9、Bcl-2、Ezrin蛋白表达及促进Bax蛋白表达有关,且浓度越高,抑制或促进作用越明显。 相似文献
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Liang Shang Pingshuan Dong Laijing Du Xuming Yang Honglei Wang Shangyang Li 《Biochemical and biophysical research communications》2019,508(1):256-262
The endoplasmic reticulum (ER) stress plays an important role in myocardial ischemia/reperfusion (MI/R) injury. SERP1, the stress-associated endoplasmic reticulum protein 1, is involved in regulating ER stress response. However, whether it associates with MI/R injury is not identified. Here, we show that SERP1 is induced in the mouse heart after MI/R injury as well as in H9c2 cells under hypoxia/reoxygenation (H/R) treatment. Additionally, SERP1 overexpression reduces H/R-induced H9c2 apoptosis. Moreover, SERP1 overexpression suppresses H/R-induced ER stress and activates JAK2/STAT3 pathway. Furthermore, JAK2/STAT3 pathway inhibition by the specific inhibitor JSI-124 minimizes the suppressive effect of SERP1 overexpression on H/R-induced ER stress and H9c2 apoptosis. Together, these results uncover the protection of SERP1 against H/R-induced H9c2 apoptosis and further relate it to JAK2/STAT3 pathway-dependent attenuation of ER stress. This study suggests SERP1 as a potential regulator invovled in the pathophysiology of MI/R injury. 相似文献