1. 细胞的基础信息

2. 细胞常见的研究有哪些？

a) 研究肝脏的生物学特性

b) 药物筛选及肝脏相关疾病治疗的研发

c) 有关该肝细胞耐药机制的研究

d) 建立细胞模型

3. 细胞相关的文献有哪些？

[1] 李玉锋,袁源,张庆,等.茶氨酸对酒精诱导人肝HL7702细胞损伤的保护作用及机理[J].西华大学学报(自然科学版),2020,39(06):87-93.

（目的：探究茶氨酸在酒精诱导人肝HL7702细胞损伤方面的保护作用及机理。方法：选取500~1000mmol范围内，梯度设置为100mmol的6个酒精浓度处理组对HL7702细胞进行初步处理，选择不同浓度茶氨酸培养HL7702细胞，MTT法测定细胞的存活率以确定酒精造模浓度和茶氨酸最适浓度范围。以不同浓度茶氨酸预保护模型浓度酒精处理过的细胞，测定细胞的存活率，检测其过氧化氢（H2O2）、丙二醛（MDA）、超氧化物歧化酶活性（SOD）、谷胱甘肽过氧化物酶（GSHPX）及总抗氧化能力（T-AOC）的含量。结果：初步确定酒精造模浓度为800mmol；茶氨酸浓度在2000μg/mL以下对HL7702细胞无毒性，结合实际情况将茶氨酸给药浓度调整为200~800μg/mL；与模型组相比，茶氨酸显著提高了酒精损伤模型中HL7702的存活率，对HL7702细胞内H2O2和MDA的生成起到了一定的抑制作用，而SOD、GSH-PX活性升高，T-AOC能力也增加。结论：茶氨酸在不同方面均被证明对酒精诱导人正常肝细胞氧化损伤具有保护作用。其作用机理是茶氨酸通过抑制酒精刺激下抗氧化关键酶活性的降低及氧化反应中间产物的产生，避免人正常肝细胞在酒精诱导下发生氧化损伤及氧化应激反应。关键词：茶氨酸；氧化损伤；HL7702；酒精性肝病）

[2] Peng H, You L, Yang C, et al. Ginsenoside Rb1 Attenuates Triptolide-Induced Cytotoxicity in HL-7702 Cells via the Activation of Keap1/Nrf2/ARE Pathway. Front Pharmacol. 2022;12:723784.

（Triptolide (TP) is the major bioactive compound extracted from Tripterygium wilfordii Hook F. It exerts anti-inflammatory, antirheumatic, antineoplastic, and neuroprotective effects. However, the severe hepatotoxicity induced by TP limits its clinical application. Ginsenoside Rb1 has been reported to possess potential hepatoprotective effects, but its mechanism has not been fully investigated. This study was aimed at investigating the effect of ginsenoside Rb1 against TP-induced cytotoxicity in HL-7702 cells, as well as the underlying mechanism. The results revealed that ginsenoside Rb1 effectively reversed TP-induced cytotoxicity in HL-7702 cells. Apoptosis induced by TP was suppressed by ginsenoside Rb1 via inhibition of death receptor-mediated apoptotic pathway and mitochondrial-dependent apoptotic pathway. Pretreatment with ginsenoside Rb1 significantly reduced Bax/Bcl-2 ratio and down-regulated the expression of Fas, cleaved poly ADP-ribose polymerase (PARP), cleaved caspase-3, and -9. Furthermore, ginsenoside Rb1 reversed TP-induced cell cycle arrest in HL-7702 cells at S and G2/M phase, via upregulation of the expressions of cyclin-dependent kinase 2 (CDK2), cyclin E, cyclin A, and downregulation of the expressions of p53, p21, and p-p53. Ginsenoside Rb1 increased glutathione (GSH) and superoxide dismutase (SOD) levels, but decreased the reactive oxygen species (ROS) and malondialdehyde (MDA) levels. Pretreatment with ginsenoside Rb1 enhanced the expression levels of nuclear factor-erythroid 2-related factor 2 (Nrf2), total Nrf2, NAD(P)H: quinone oxidoreductases-1 (NQO-1), heme oxygenase-1 (HO-1), and Kelch-like ECH-associated protein 1 (Keap1)/Nrf2 complex. Therefore, ginsenoside Rb1 effectively alleviates TP-induced cytotoxicity in HL-7702 cells through activation of the Keap1/Nrf2/ARE antioxidant pathway. Keywords: HL-7702 cells; Keap1/Nrf2/ARE pathway; apoptosis; cytotoxicity; ginsenoside Rb1; triptolide.）