INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
·
2025
·Vol. 26
·期 5
·2118
·
IF 4.9
Xiyue Wang,Miaoyunhuan Wang,Yuqing Dong,Shuqing Yu,Shanshan Zhang,Pinghua Sun,Lu Wang,Jibin Liu,Houwen Lin,Xinhui Pan,Xiaobin Li
Chenopodium albumL., as a folkloric herb, is traditionally used to treat poisonous insect bites, vitiligo, and other ailments. However, its impact on thrombosis remains unknown. In this study, we discovered that the ethanol extract ofC. albumexhibited a remarkable antithrombotic effect using a zebrafish thrombosis model for the first time. Activity evaluation showed that fraction CA-C could improve thrombus aggregation in the caudal vein, increase blood return in the heart, and alleviate the slowing of blood flow compared with those in the model group. Then, analysis by ultra-high performance liquid chromatography-quadrupole time-of-flight tandem mass (UPLC-Q-TOF-MS) identified 58 constituents of CA-C, with most of them belonging to flavonoids, alkaloids, and steroidal saponin components. Moreover, using a comprehensive strategy of network pharmacological analysis, transcriptomic assay, and RT-qPCR validation, we found that CA-C could mediate the TLR’s signaling pathway and its downstream MAPKs and PI3K/AKT signaling pathways to exert an antithrombotic effect. This study broadens the clinical application of plantC. albumand provides new insight into the chemical profile, pharmacodynamics, and potential mechanisms of CA-C as candidate agents for treating thrombosis.
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高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
·
2017
·
IF 2.981
Zhongcheng Ke,Gang Wang,Lei Yang,Huihui Qiu,Hao Wu,Mei Du,Juan Chen,Jie Song,Xiaobin Jia,Liang Feng
Ethnopharmacological relevance Radix paeoniae rubra , also known as chishao (CS), is a frequently used traditional Chinese medicine that can promote blood circulation to remove blood stasis . It has been widely used for the prevention and treatment of cardiovascular diseases in China. Although terpene glycoside (TG), the major component in CS, has been shown to possess cardioprotective properties, the mechanism underlying CS-TG's preventive effect against myocardial ischemia injury is unknown. This study was conducted to explore the protective and curative effects of CS-TG against isoproterenol (ISO)-induced myocardial ischemic injury in rats and investigate the underlying myocardial protective mechanisms. Materials and methods A rat model of ISO-induced myocardial ischemia was established to evaluate the protective effect of CS-TG in ameliorating heart injury. Myocardial ischemia was induced by administering ISO (40 mg/kg/d) subcutaneously for 2 days. Serum was collected and analyzed for the levels of different cardiac biomarkers, and heart tissues were isolated and prepared for ATP analysis, glycogen content determination, histopathology assay, and ultrastructure observation. The regulatory effects of CS-TG on myocardial apoptosis in rats were studied by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, and the levels of cleaved caspase-3, Bax, and Bcl-2 were detected by western blotting . Furthermore, in vitro experiments were conducted to examine whether the CS-TG's cardioprotective effects were linked to the inhibition of apoptosis via activation of the phosphoinositide-3-kinase/serine-threonine kinase AKT/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway. Results CS-TG (300 mg/kg/d) significantly decreased serum levels of creatine kinase and lactate dehydrogenase in ISO-induced myocardial ischemic rats. Analysis of ATP and glycogen contents, myocardial ultrastructure, and pathological examination showed that CS-TG (300 mg/kg/d) significantly improved energy metabolism and alleviated myocardial injury in vivo. In addition, the expression of p-AKT and p-mTOR in rats subjected to CS-TG significantly elevated, while the levels of caspase-3 and Bax/Bcl-2 dramatically reduced. Moreover, treatment with LY294002 , a PI3K inhibitor, abrogated CS-TG (200 μg/mL) induced down-regulation of cleaved caspase-3, Bax/Bcl-2 in the serum. Conclusions CS-TG protects the heart from ISO-induced myocardial ischemia, potentially by improving cardiac energy metabolism and inhibiting cardiomyocyte apoptosis via activation of the PI3K/AKT/mTOR signaling pathway. Thus, CS -TG might be a potential therapeutic candidate for the prevention and treatment of myocardial ischemia.
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Heliyon
·
2024
·
IF 3.4
Chunhua Liu,Yu He,Kun Zhou,Hong Wang,Meng Zhou,Jia Sun,Yuan Lu,Yong Huang,Yonglin Wang,Ting Liu,Yongjun Li
Background Gerberae Piloselloidis Herba (GPH) exhibits notable efficacy in alleviating allergic asthma. Previous studies in our research have identified a mixture of luteolin, arbutin, and marmesin as effective components of GPH in treating allergic asthma. However, the underlying mechanism remains unclear. This study aims to elucidate the molecular mechanism of these active components. Method Using an ovalbumin (OVA)-induced allergic asthma mouse model, various treatment groups were administered, including GPH, the active component mixture (termed "Mixture") containing luteolin, arbutin, and marmesin, and a positive drug (dexamethasone, DEX). Relevant indices were assessed, including behavioral characteristics, inflammatory cell counts, cytokine levels, histopathological examination of lung tissue, apoptosis, and expression of key proteins such as Caspase-3, Bax, Bcl-2, PI3K, p-PI3K, Akt, and p-Akt. The effect of the Mixture on the PI3K/Akt signaling pathway was further verified using the PI3K inhibitor LY294002. Results The Mixture significantly alleviated asthma symptoms, decreased IgE levels, cytokine levels (IL-4, IL-5, IL-13 and TNF-α), and the number of inflammatory cells in serum or bronchoalveolar lavage fluid (BALF), leading to the alleviation of lung pathological lesions. Additionally, the Mixture reduced the expression of Bax and Caspase-3 while increasing Bcl-2 expression, resulting in mitigated apoptosis in lung tissue. Furthermore, there appeared a decrease in the levels of PI3K and p-PI3K, as well as the ratio of p-Akt to Akt in the Mixture group, indicating the suppression of PI3K and Akt phosphorylation. Interestingly, the effects of the Mixture were comparable to those of GPH, LY294002, or the combination of LY294002 with the Mixture. Conclusion The study confirms that the Mixture containing luteolin, arbutin, and marmesin indeed alleviates allergic asthma induced by OVA in mice by suppressing the PI3K/Akt signaling pathway. These findings highlight the potential of the GPH-derived Mixture as a novel therapeutic for the treatment of allergic asthma.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2025
·
IF 8.5
Donglei Zheng,Lulu Ma,Xiaojuan Xin,Ying Gao,Shijian Dong,Ying Huang,Jijun Wu,Jiaying Huo,Shugang Li
Ovotransferrin (OVT), a bioactive protein from egg white, has been demonstrated to exhibit anti-inflammatory efficacy and suppress the progression of ulcerative colitis. Nevertheless, its role in preserving intestinal barrier integrity has not been reported. This study investigated the role of OVT on intestinal barrier dysfunction in DSS-induced ulcerative colitis mice and its underlying mechanisms. OVT significantly attenuated the severity of intestinal barrier injury, reduced inflammatory infiltration, and restored goblet cell density (Model: 5.00 goblet cells/crypt, High: 12.75 goblet cells/crypt) alongside the expression of MUC2 (87.64 %), ZO-1 (83.98 %), and Occludin (74.93 %). Concurrently, OVT decreased intestinal permeability by 84.42 %. Furthermore, OVT downregulated pro-inflammatory cytokines (TNF-α, IL-1β, IL-6), while elevating anti-inflammatory IL-10 levels and restoring redox homeostasis. RNA-seq and Western blot analysis revealed that OVT inhibited the PI3K-Akt/MAPK pathway by decreasing the phosphorylation of p85α (31.73 %), Akt (69.59 %), p38 (25.00 %), and ERK (41.18 %). Metabolomics showed that OVT modulated key metabolites, including L-glutamate, serotonin, and d -fructose-6-phosphate, while decreasing glucose and L-asparagine. These results suggested that OVT regulated immune responses and metabolic pathways, highlighting its therapeutic potential in preserving intestinal barrier integrity.
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ONCOLOGY REPORTS
·
2023
·Vol. 51
·期 1
·1-13
·
IF 4.2
Gongjie Ye,Linglan Tu,Zhuduo Li,Xiangyu Li,Xiaoliang Zheng,Yongfei Song
Synaptopodin 2 (SYNPO2) plays a pivotal role in regulating tumor growth, development and progression in bladder urothelial Carcinoma (BLCA). However, the precise biological functions and mechanisms of SYNPO2 in BLCA remain unclear. Based on TCGA database‑derived BLCA RNA sequencing data, survival analysis and prognosis analysis indicate that elevated SYNPO2 expression was associated with poor survival outcomes. Notably, exogenous SYNPO2 expression significantly promoted tumor invasion and migration by upregulating vimentin expression in BLCA cell lines. Enrichment analysis revealed the involvement of SYNPO2 in humoral immune responses and the PI3K/AKT signaling pathway. Moreover, increased SYNPO2 levels increased the sensitivity of BLCA to PI3K/AKT pathway‑targeted drugs while being resistant to conventional chemotherapy. In in vivo BLCA mouse models, SYNPO2 overexpression increased pulmonary metastasis of 5637 cells. High SYNPO2 expression led to increased infiltration of innate immune cells, particularly mast cells, in both nude mouse model and clinical BLCA samples. Furthermore, tumor immune dysfunction and exclusion score showed that patients with BLCA patients and high SYNPO2 expression exhibited worse clinical outcomes when treated with immune checkpoint inhibitors. Notably, in the IMvigor 210 cohort, SYNPO2 expression was significantly associated with the population of resting mast cells in BLCA tissue following PD1/PDL1 targeted therapy. In conclusion, SYNPO2 may be a promising prognostic factor in BLCA by modulating mast cell infiltration and exacerbating resistance to immune therapy and conventional chemotherapy.
研究领域:
肿瘤学
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免疫学
·
分子生物学
·
癌症生物学
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PubMed
高影响因子
PHYTOMEDICINE
·
2024
·
IF 6.7
Lin Chen,Xin Kong,Ruina Zhou,Jinhang Hu,Rui Zhou,Zhongxing Song,Zhishu Tang,Mei Wang
ABSTRACT Background Total flavonoids from Astragali Complanati Semen (TFACS), the main active ingredients in Astragali Complanati Semen (ACS), have been shown to have a protective effect on chronic liver injury (CLI), but the hepatoprotective targets and signalling pathways involved are unclear. Purpose The aim of our study was to identify the anti-CLI targets and signalling pathways of TFACS and to comprehensively elucidate its mechanism of action via proteomics analysis combined with in vivo and in vitro experiments. Methods A CLI mouse model was generated via intraperitoneal injection of carbon tetrachloride (CCl 4 ) (CCl 4 : olive oil = 1:4, 2 mL/kg, twice a week for 6 weeks). The hepatoprotective effect of TFACS was assessed by observing the pathological structure of the liver and analysing indicators of liver function. The key pathways and targets related to the hepatoprotective effect of TFACS were identified via 4D-label-free quantitative proteomics technology and further verified via in vivo indicator validation and in vitro cell experiments. Results TFACS administration significantly normalized the histopathological structure and function of the liver, decreased the levels of inflammatory factors and oxidative stress indicators, and reduced the iron staining area and the levels of hepcidin and iron in the liver compared with those in the CLI model. A total of 424 differentially expressed proteins (DEPs) were identified between the TFACS and model groups, and these DEPs were enriched in the focal adhesion, PI3K-Akt, and ferroptosis pathways. Akt1, Pik3ca, NF-κB p65, Itga5, Itgb5, Itga6, Prkca, Fn1, Tfrc, and Vdac3 were identified as key targets of TFACS. TFACS administration significantly reversed the changes in the gene and protein expression of the key targets compared with those in the model group. In addition, TFACS treatment significantly reduced the levels of inflammatory cytokines and inhibited Akt1, NF-κB p65 and FAK activation in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages. In an erastin-induced L-O2 ferroptosis cell model, treatment with TFACS normalized the mitochondrial structure, reduced the protein levels of Tfrc and Vdac3, inhibited lipid peroxidation, and reduced the amount of Fe 2+ in the mitochondria. Conclusion TFACS protected against CLI, and its mechanism of action may be related to inhibition of the focal adhesion, PI3K/Akt and ferroptosis signalling pathways.
研究领域:
药理学
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蛋白质组学
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肝病学
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高影响因子
Frontiers in Pharmacology
·
2024
·
IF 4.4
Li Yan,Ge Jingping,Yin Yuanyuan,He Juan,Shang Longcheng
Background: This study aimed to explore the regulatory effect of anserine on HUVEC cell injury and thrombosis in deep venous thrombosis (DVT) rats, and to elucidate the underlying molecular mechanisms.Methods: Non-targeted metabolomics data analyses were conducted using an ultra-performance liquid chromatography system Vanquish UHPLC and mass spectrometer to detect plasma metabolism profiles. The transcriptome sequencing and gene intervention experiments were performed to verify the regulatory effect. Further in vivo and in vitro experiments were performed. Enzyme-linked immunosorbent assay was used to detect the levels of P-selectin, E-selectin, and vWF, hematoxylin-eosin (HE) staining was performed to observe thrombotic and inflammatory cell infiltration, flow cytometry and TUNEL assays were performed to detect apoptosis, and qPCR and WB assays were conducted to determine the gene and protein expression.Results: Anserine alleviated HUVECs injury, reduced adhesion molecule expression, and inflammation. It decreased P-selectin, E-selectin, vWF, THBD, TFPI levels, and apoptosis while promoting NOS3, ET-1, and NO release in HUVECs. In DVT rats, anserine reduced P-selectin, E-selectin, vWF, thrombosis, cell infiltration, apoptosis, and promoted NO release. Transcriptome sequencing and gene intervention confirmed anserine’s regulation of the PI3K-Akt pathway and coagulation via MYB. CARNMT1, a regulatory enzyme for anserine metabolism, increased anserine content, inhibiting coagulation, thrombosis, cell infiltration, and promoting NO release in rats.Conclusion: This study confirmed anserine could alleviate DVT by improving the inflammatory response, inhibiting blood agglutination, and promoting vasodilation, providing new potential therapeutic targets, important scientific evidence for the development of DVT management, and new clues for an in-depth understanding of its molecular mechanisms.
研究领域:
药理学
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分子生物学
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心血管疾病
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血栓
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Cancer Cell International
·
2021
·Vol. 21
·期 1
·1-15
·
IF 5.722
Lv Minchao,Xu Qingxin,Zhang Bei,Yang Zhiqiang,Xie Jun,Guo Jinku,He Feixiong,Wang Wei
Background Osteosarcoma is the third most common cancer in adolescence and the first common primary malignant tumor of bone. The long-term prognosis of osteosarcoma still remains unsatisfactory in the past decades. Therefore, development of novel therapeutic agents which are effective to osteosarcoma and are safe to normal tissue simultaneously is quite essential and urgent. Methods Firstly, MTT assay, cell colony formation assay, cell migration and invasion assays were conducted to evaluate the inhibitory effects of imperatorin towards human osteosarcoma cells. RNA-sequence assay and bioinformatic analysis were then performed to filtrate and assume the potential imperatorin-induced cell death route and signaling pathway. Moreover, quantitative real-time PCR assay, western blot assay and rescue experiments were conducted to confirm the assumptions of bioinformatic analysis. Finally, a subcutaneous tumor-transplanted nude mouse model was established and applied to evaluate the internal effect of imperatorin on osteosarcoma by HE and immunohistochemistry staining. Results Imperatorin triggered time-dependent and dose-dependent inhibition of tumor growth mainly by inducing autophagy promotion and G0/G1 phase arrest in vitro and in vivo. Besides, imperatorin treatment elevated the expression level of PTEN and p21, down-regulated the phosphorylation of AKT and mTOR. In contrast, the inhibition of PTEN using Bpv (HOpic), a potential and selective inhibitor of PTEN, concurrently rescued imperatorin-induced autophagy promotion, cell cycle arrest and inactivation of PTEN-PI3K-AKT-mTOR/p21 pathway. Conclusions This work firstly revealed that imperatorin induced autophagy and cell cycle arrest through PTEN-PI3K-AKT-mTOR/p21 signaling pathway by targeting and up-regulating PTEN in human osteosarcoma cells. Hence, imperatorin is a desirable candidate for clinical treatments of osteosarcoma.
研究领域:
肿瘤学
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药理学
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细胞生物学
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分子生物学
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高影响因子
DRUG DEVELOPMENT RESEARCH
·
2021
·Vol. 83
·期 1
·64-74
·
IF 4.36
Yang Yang,Tao Cheng,Peng Xie,Lishan Wang,Hong Chen,Zhangjun Cheng,Jiahua Zhou
To explore the biological activity of transmembrane prostateandrogen induced RNA (PMEPA1) in human pancreatic cancer (hPAC) cells and its drug sensitivity to gemcitabine (GEM) and cisplatin (DDP). Gene Expression Profiling Interactive Analysis (GEPIA) and Cancer Cell Line Encyclopedia (CCLE) were consulted to indicate the expression of PMEPA1 in hPAC tissues and cells. Quantitative real-time PCR (RT-qPCR) and western blot were performed to verify the indication. RT-qPCR and western blot also detected the expressions of PTEN/PI3K/AKT before and after transfection of PMEPA1 siRNA plasmids. Cell counting Kit-8 (CCK-8) and EdU staining were performed to examine cell proliferation before and after transfection of phosphatase and tensin homologue delet2ed on chromosome ten (PTEN) siRNA plasmids. Transwell and wound healing detected the invasion and migration of hPAC cells. The expressions of MMP-2 and MMP-9 were detected by western blot. After GEM or DDP treatment, cell viability was observed by commercial kits and cell apoptosis by flow cytometry. GEPIA and CCLE predicted increased expression of PMEPA1 in hPAC tissues and cells, which was confirmed by quantitative reverse transcription polymerase chain reaction (RT-qPCR) and western blot. PMEPA1 was also shown to be associated with disease-free survival. Transfection of PMEPA1 siRNA plasmids affected the expressions of PTEN/PI3K/AKT. PMEPA1 interference inhibited the proliferation, invasion and migration of hPAC cells. Furthermore, PMEPA1 interference also enhanced the sensitivity of hPAC cells to GEM and DDP via PTEN interference. PMEPA1 interference inhibits the proliferation, invasion and migration of pancreatic cancer cells and enhances the sensitivity to GEM and cisplatin by activating PTEN/PI3K/AKT signaling.
研究领域:
肿瘤学
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分子生物学
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细胞生物学
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高影响因子
BMC Pregnancy and Childbirth
·
2026
·Vol. 26
·期 1
·363
·
IF 3.1
Xie Xinping,Yan Jianying,Chen Xiaoyun,He Lidan,Wu Jianbo,Lu Lin
Background Insulin resistance (IR) is a pivotal determinant in the pathophysiological processes underlying gestational diabetes mellitus (GDM). Angiopoietin-like protein 8 (ANGPTL8) exhibits an ambiguous influence on glucose metabolism in the onset and progression of GDM. However, the functions of ANGPTL8 in the metabolic profiles of insulin-resistant (IR) HepG2 cells, glucose tolerance in GDM mice, and the possible underlying mechanisms require further exploration. Methods ANGPTL8 knockout and over-expressing HepG2 cell lines were established. Glucose uptake capacity in three clones (wild-type, ANGPTL8 knockout, and over-expressing) of insulin-resistant HepG2 cells was detected. Proteomic analysis of the IR HepG2 cells identified a cluster of relevant signaling pathways, and the effect of ANGPTL8 on metabolomic changes was evaluated. The GDM model was induced by a high-fat diet (HFD) and intraperitoneal injection of Streptozotocin (STZ) in pregnant mice. An oral glucose tolerance test (OGTT) was performed in both GDM mice and ANGPTL8 over-expressing GDM mice. Results The PI3K/Akt signaling cascade was stimulated by insulin resistance, and this activation could be effectively suppressed by inhibitors targeting PI3K, Akt, and GSK-3β. HepG2 cells over-expressing ANGPTL8 and exposed to high insulin concentrations demonstrated a marked enhancement in glucose uptake capacity, as opposed to their wild-type counterparts or ANGPTL8 knockout cells under IR conditions. The most substantial down-regulation was observed in lactate and branched-chain amino acids (BCAAs), which exhibited a positive correlation with IR. Promoted translation of ANGPTL8 was found in the liver, pancreas, and placental tissues of GDM mice. Significantly better glucose tolerance was observed in GDM mice transfected with m-ANGPTL8 compared with those that were not. Furthermore, the activation of Akt was observed in the primary hepatocytes of ANGPTL8 over-expressing GDM mice. Conclusion Over-expression of ANGPTL8 may increase glucose uptake capacity and influence the metabolic profiles in IR HepG2 cells, enhancing the insulin-mediated activation of the PI3K/Akt/GSK-3β pathway. ANGPTL8 may improve glucose tolerance in GDM mice. These findings might contribute to a new understanding of the roles of ANGPTL8 in glucose metabolism during the onset and progression of insulin resistance, providing novel insights for the clinical therapy of GDM.
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Food Bioscience
·
2026
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IF 6.2
Xiao Qiang,Mengyuan Gao,Zongshuo Li,Weidong Li
SQLE is a potential functional food for alleviating spleen deficiency syndrome. • SQLE contains diverse bioactive compounds with flavonoids as major components. • SQLE restores gut microbiota homeostasis and promotes SCFAs production. • SQLE improves spleen deficiency via the PI3K/Akt/NF-κB/AQP3 signaling pathway. Spleen deficiency syndrome (SDS) manifests as impaired digestive function, fatigue, and metabolic issues, which are closely associated with dysbiosis of the gut microbiota. Shen-Qi-Ling extract (SQLE) is a natural extract prepared from food-medicine homologous resources, primarily consisting of Codonopsis pilosula , Astragalus membranaceus , and Poria cocos . However, the bioactive constituents and mechanisms by which it alleviates SDS remain unclear. In this study, we systematically characterized the chemical constituents of SQLE and elucidated its potential mechanisms of action against SDS in mice. Using ultra-high-performance liquid chromatography coupled with tandem mass spectrometry (UPLC-MS/MS) analysis, 137 compounds were identified in SQLE, with flavonoids being the most abundant, followed by coumarins, phenylpropanoids, and organic acids. Molecular docking analysis indicated that SQLE might have a spleen-strengthening effect. Treatment with SQLE, particularly SQLE-M, significantly enhanced intestinal absorption, exercise performance, tissue damage, and oxidative stress. Moreover, SQLE-M restored gut microbial homeostasis, increased the relative abundance of potentially beneficial bacteria, and promoted the production of short-chain fatty acids (SCFAs). Notably, SQLE-M normalized the intestinal barrier dysfunction and metabolic disorders by activating the PI3K/Akt signaling pathway, inhibiting NF-κB-mediated inflammatory responses, and upregulating aquaporin 3 (AQP3) expression. Collectively, SQLE mitigates SDS, which may be associated with alterations in the gut microbiota-metabolite axis and the PI3K/Akt/NF-κB/AQP3 signaling pathway, offering new perspectives for developing spleen-strengthening functional foods derived from food-medicine homologous resources. Download: Download high-res image (462KB) Download: Download full-size image
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Frontiers in Pharmacology
·
2022
·
IF 5.988
Sun Jia-Yi,Liu Yi-Tong,Jiang Sheng-Nan,Guo Peng-Mei,Wu Xin-Yu,Yu Jia
For thousands of years, the roots of Paeonia lactiflora Pall (PLP) has been considered by traditional Chinese medicine as a drug that can improve mental or emotional disorders, including depression, anxiety and affective disorders. Unfortunately, the research on the mechanism of action and active ingredients of this beneficial drug is not comprehensive. This study focused on the activity of essential oil from PLP (EOP), systematically studied the antidepressant effect of EOP for the first time, and discussed the potential mechanism of its antidepressant effect. In this study, we used a mouse model of corticosterone (CORT)-induced depression, and found that EOP had a significant antidepressant effect on the symptoms of CORT-induced depression in mice, and significantly down-regulated the levels of CRH, ACTH and cortisol in the brain tissues of mice. In addition, we found that EOP treatment alleviated CORT-induced hippocampal neuron injury in mice In vitro experiments. It was also found that EOP could inhibit CORT-induced apoptosis and improve the proliferation ability and cell viability of PC12 cells. Further, with the help of network analysis, it was revealed that PI3K-Akt might be one of the main signaling pathways of EOP against CORT-induced hippocampal neuron apoptosis. In this study, we also found that EOP up-regulated the phosphorylation of PI3K and Akt in CORT-induced mouse hippocampal neurons and PC12 cells, and promoted the nuclear transcription of Nrf2 in CORT-induced PC12 cells. In conclusion, with the integrated approach, we demonstrated that EOP exerted anti-apoptotic effects on hippocampal neurons through PI3K/Akt/Nrf2 signaling pathway.
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