目的 初步探讨黄芩苷防治支气管哮喘的作用机理。方法 用卵蛋白致敏大鼠制备支气管哮喘动物模型,经黄芩苷干预治疗,运用免疫组化法及Western Blot法检测各组大鼠肺组织匀浆中p38 MAPK磷酸化蛋白表达量。结果 两种检测方法均显示,p38 MAPK磷酸化蛋白水平在模型组中有明显的增加,地塞米松组、黄芩苷高剂量组和低剂量组的p38 MAPK磷酸化蛋白水平均低于模型组(P<0.05)。结论 黄芩苷能有效治疗哮喘的作用与抑制哮喘大鼠p38 MAPK信号通路的表达密切相关。

Objective To explore the mechanism of Baicalin in treatment of bronchia asthma. Methods Animal models of bronchia asthma were made in rats sensitized with egg albumen. After the treatment of Baicalin, immunohistochemistry and western-blot methods were used to test expression quantity of phosphorylated p38 protein of lung tissue in all groups of guinea rats. Results Our data confirmed that the level of phosphorylated p38 protein increased significantly in model group, but it decreased in hexadecadrol group, high dose and low dose Baicalin group (P<0.05). Conclusion The effects of Baicalin in asthma model were associated with inhibition of P38 MAPK signal pathways in a dose-dependent manner.

目的 观察鼻咽癌患者癌组织中RhoA蛋白-Rho激酶蛋白表达情况。方法 收集增城市人民医院2009年2月—2014年6月耳鼻喉科住院治疗,进行活检的鼻咽癌患者切除标本共62例,包括癌组织及癌旁组织。通过SABC免疫组织化学法检测患者癌组织及癌旁组织中RhoA蛋白-Rho激酶蛋白表达情况。结果 鼻咽癌组织RhoA蛋白阳性表达率及Rho激酶蛋白阳性率高于癌旁组织(P=0.00);鼻咽癌癌组织RhoA及Rho激酶表达在年龄及性别分布上无差异,而TNM分期中Ⅲ期+Ⅳ期RhoA及Rho激酶表达阳性率高于Ⅰ期+Ⅱ期患者,同时存在淋巴结转移患者其RhoA及Rho激酶表达阳性率高于未转移患者。结论 鼻咽癌患者癌组织中RhoA蛋白及Rho激酶表达阳性率高,TNM分期越高及存在淋巴结转移者其RhoA蛋白及Rho激酶表达阳性率越高。RhoA-Rho激酶信号通路参与了鼻咽癌发生发展的过程。

Objective To observe the expression of RhoA-Rho kinase protein in patients with nasopharyngeal carcinoma tissue. Methods Collecting 62 cases of patients with nasopharyngeal carcinoma who hospitalized and hadbiopsyof specimens, including carcinoma tissues and adjacent tissues in department of otolaryngology-head and neck surgery from February 2010 to October 2014. The expression of RhoA-Rho kinase protein in carcinoma tissues and adjacent tissues was detected with SABC immune histochemical method. Results Positive expression rate of nasophryngeal carcinoma tissue RhoA protein and Rho kinase protein was significantly higher than that of adjacent tissues, and there was no obvious difference in age and sex between the expression of nasopharyngeal carcinoma tissue RhoA and Rho kinase(P=0.00), while patients being in the third and fourth periods of TNM stage had a higher positive expression rate of RhoA and Rho kinase than those being in the first and second periods. At the same time, RhoA and Rho kinase positive expression rate in patients with lymph node metastasis was higher than that in those without lymph node metastasis. Conclusion Positive expression rate of RhoA protein and Rho kinase in patients with nasopharyngeal carcinoma. The higher TNM stage is, the higher positive expression rate of RhoA protein and Rho kinase in lymph node metastasis is. RhoA-Rho kinase signaling pathways involved in the occurrence and development of nasopharyngeal carcinoma.

       目的   研究SOCS6/STAT6通路在前列腺细胞炎性增殖作用中的调控作用。方法  使用人前列腺细胞株RWPE-1建立炎症模型，将细胞分为对照（CON）组和炎症刺激（INF）组，后者通过添加脂多糖（LPS）模拟炎症环境。采用ELISA检测白细胞介素-1β（IL-1β）-1β、白细胞介素-6（IL-6）和白细胞介素-8（IL-8）表达水平，蛋白免疫印迹法检测细胞因子信号抑制物-6（SOCS6）、信号转导和转录激活因子-6（STAT6）及磷酸化STAT6蛋白的表达水平。结果  经过LPS处理后，RWPE-1细胞中的SOCS6蛋白表达水平显著下降（P＜0.01），而磷酸化STAT6表达水平上升（P＜0.01）。结论  SOCS6/STAT6通路可能通过调节炎症环境下STAT6的磷酸化水平，参与调节前列腺细胞的炎性增殖作用。

       Objective   To explore the  regulatory  role of  SOCS6/STAT6  pathway in the inflammatory  proliferation of 

prostate cells．Methods  The human prostate cell line RWPE-1 was used to establish an inflammation model．Cells were divided into a control（CON）group and an inflammation-stimulated（INF）group，with the latter subjected to lipopolysaccharide（LPS）treatment to simulate an inflammatory environment．The expression levels of interleukin（IL）-1β、IL-6 and  IL-8 were detected by ELISA，and the expression levels of suppressor of cytokine signaling 6（SOCS6），signal transducer and activator oftranscription-6，（STAT6），and phosphorylated STAT6 proteins were detected by Western blot．Results  The  results showed that after LPS treatment，the expression of SOCS6 protein in RWPE-1 cells significantly decreased，while the expression of phosphorylated STAT6 increased．Conclusions  The SOCS6/STAT6 pathway may be involved in  regulating the inflammatory proliferation of prostate cells by modulating the phosphorylation level of STAT6 under inflammatory conditions．

       目的   探讨谷氨酸对HT22细胞线粒体自噬和细胞凋亡的影响，并评估虾青素预处理的保护作用及其分子机制。方法   用谷氨酸及虾青素处理HT22细胞，通过蛋白印迹及聚合酶联反应等评估其对线粒体自噬的影响。结果   谷氨酸处理显著抑制线粒体初级自噬（PINK1、Parkin、pULK1^ser555和LC3Ⅱ）和次级自噬（LAMP1和Rab7），上调cleaved Caspase-3的表达（P＜0.05）。虾青素预处理减少细胞凋亡，恢复了线粒体自噬，PINK1、Parkin、pULK1^ser555和LC3Ⅱ的表达水平上升（分别为2.3倍、2.6倍、83.3%及81.1%）（P＜0.05），该作用被自噬抑制剂BafA1阻断。此外，谷氨酸抑制Nrf2核内转移和NLRX1表达，而预处理显著促进Nrf2的核内转移并上调NLRX1，分别上调25.8%、33.2%。生物信息学分析显示NLRX1启动子区域含有3个Nrf2结合位点，提示Nrf2通过调控NLRX1转录活性发挥作用。结论   文章揭示虾青素通过Nrf2/NLRX1通路激活线粒体自噬，展现神经保护作用。

       Objective  To explore the effects of glutamate on mitophagy and apoptosis in HT22 cells and evaluate the protective effects and molecular mechanisms of astaxanthin pretreatment．Methods  HT22 cells were treated with glutamate and astaxanthin．The effects on mitophagy were assessed using Western Blot and PCR．Results  Glutamate treatment  significantly inhibited primary mitophagy（PINK1，Parkin，pULK1^ser555 and LC3II）and secondary mitophagy（LAMP1 and Rab7）while upregulating cleaved Caspase-3 expression．Astaxanthin pretreatment notably reduced apoptosis and restored mitophagy，the expression levels of PINK1，Parkin，pULK1^ser555 and LC3II were significantly upregulated（by 2.3-fold，2.6-fold，83.3% and 81.1% respectively，P＜0.05），but this effect was blocked by the autophagy inhibitor BafA1．Additionally，glutamate suppressed Nrf2 nuclear translocation and NLRX1 expression，whereas astaxanthin promoted Nrf2 nuclear translocation and increased NLRX1 expression by 25.8% and 33.2%，respectively．Bioinformatics analysis  revealed three Nrf2 binding sites in the NLRX1 promoter region，suggesting that Nrf2 may regulate NLRX1 transcriptional activity．Conclusions  The study demonstrates that astaxanthin exhibited potential neuroprotective effect by activating mitophagy through the Nrf2/NLRX1 pathway．

       目的  探讨重楼皂苷Ⅰ（PPI）对慢性髓系白血病细胞（K562）细胞的抑制作用及可能的作用机制。方法  采用CCK-8法筛选药物最适浓度，将培养时间为24 h的药物最适浓度作为后续实验的干预浓度。分组如下：（1）空白组；（2）PPI组；（3）抑制剂组；（4）PPI+抑制剂组。采用CCK-8法检测细胞增殖率；AO/EB染色观察细胞形态；流式细胞术检测凋亡率；ROS检测试剂盒检测活性氧（ROS）含量、还原型谷胱甘肽含量检测试剂盒检测谷胱甘肽（GSH）含量、细胞亚铁比色法测试盒检测细胞亚铁（Fe²⁺）含量；qRT-PCR法和蛋白免疫印迹法检测各组肿瘤蛋白53（p53）、钠氯离子依赖性氨基酸转运蛋白11（SLC7A11）、谷胱甘肽过氧化物酶4（GPX4）mRNA及蛋白表达量。结果  PPI抑制K562细胞的生长，且呈一定的剂量及时间依赖性（与同时间段的对照组0μmol/L比较，均P＜0.01）。与空白组相比，PPI抑制K562细胞的增殖，提高了凋亡率，而铁死亡抑制剂（Ferrostian-1）的使用逆转了PPI对K562凋亡的促进作用（P＜0.01）。与空白组相比，PPI组ROS、Fe²⁺含量升高，GSH含量下降，而铁死亡抑制剂的使用可下调ROS、Fe²⁺，上调GSH的含量（P＜0.01）。PPI组较空白组p53 mRNA和蛋白表达水平升高，而SLC7A11、GPX4 mRNA和蛋白表达水平下降（P＜0.05）；PPI+抑制剂组细胞较重楼皂苷组p53 mRNA和蛋白表达水平下降，而SLC7A11、GPX4 mRNA和蛋白表达水平升高（P＜0.05）。结论  PPI能够有效抑制K562细胞增殖，促进K562细胞铁死亡，其分子机制可能与p53信号通路的调控有关。

       Objective  To investigate the inhibitory effect of polyphyllin I（PPI）on chronic myeloid leukemia cells（K562）and its possible mechanism．Methods  K562 cell line was cultured in suitable environment，and the optimal concentration of the drug was screened by CCK-8 method．The optimal concentration of the drug cultured for 24 hours was used as the intervention concentration of the follow-up experiment．Cells were divided into the following groups：（1）blank group，（2）saponins group，（3）inhibitor group and（4）saponins + inhibitor group．The cell proliferation rate was detected by CCK-8 method．The cell morphology was observed by AO/EB staining．The apoptosis rate was detected by flow cytometry．The contents of  reactive oxygen species（ROS），glutathione（GSH）and ferrous（Fe²⁺）in different groups were detected，and the expression of mRNA and protein in different groups were detected by qRT- PCR and Western blot respectively．Results  PPI significantly inhibited the growth of K562 cells in a dose-and time-dependent manner．Compared with the blank group，PPI significantly inhibited the proliferation of K562 cells and increased the apoptosis rate of K562 cells，while the use of ferroptosis inhibitor（Ferrostian-1）reversed the promoting effect of PPI on apoptosis of K562 cells．Compared with the blank group，the contents of reactive oxygen species（ROS）and ferrous iron（Fe²⁺）increased and the content of glutathione（GSH）decreased in the saponins group．The use of Ferrostian-1 could down-regulate the contents of ROS and Fe²⁺ and increase the content of GSH in the cells treated with the drug．Compared with the blank group，the expression of p53 mRNA and protein in the saponins group increased，while the expression of SLC7A11，GPX4 mRNA and protein decreased．The expression of p53 mRNA and protein in the saponins + inhibitor group was lower than that in the saponins group，while the expression levels of SLC7A11，GPX4 mRNA and protein increased．Conclusions  PPI can effectively inhibit the proliferation of K562 cells and promote ferroptosis in K562 cells．The molecular mechanism can be related to the regulation of p53 signal pathway．

       卵巢癌是导致女性死亡的全球第五大原因，其治疗效果受限于早期诊断和治疗方案的有限性。近年来，随着靶向治疗的不断发展，细胞死亡途径作为治疗靶点受到广泛关注，其中双硫死亡作为一种新发现的程序性细胞死亡形式，为癌症治疗提供了新的思路。文章探讨了双硫死亡及其他主要细胞死亡途径包括自噬、细胞焦亡、坏死性凋亡、铁死亡和铜死亡在卵巢癌治疗中的研究进展，有望为卵巢癌患者提供更有效的治疗选择。

    Ovarian cancer ranks as the fifth deadliest cancer among women worldwide，with treatment efficacy hampered 

by limited early diagnosis and therapeutic options．In recent years，with the continuous development of targeted therapies，cell death pathways have gained widespread attention as therapeutic targets．Among them，disulfideptosis，a newly discovered form of programmed cell death，offers a novel avenue for cancer treatment．This review aims to explore the research progress of disulfideptosis and other major cell death pathways including autophagy，apoptosis，necroptosis，ferroptosis，and cuproptosis in ovarian cancer therapy，with the potential to provide more effective treatment options for ovarian cancer patients．