BIOLOGICAL & PHARMACEUTICAL BULLETIN
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2020
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IF 1.863
Yuanguo Xiong,Hao Lu,Hanlin Xu
Hepatic fibrosis (HF) is a common disease, with currently no available treatment. Galangin, a natural flavonoid extracted from Alpinia officinaruim Hance, has multiple effects demonstrated in previous studies. The aim of the present study was to explore the anti-fibrogenic effect of galangin in vitro, and research its potential molecular mechanisms. LX-2 cells were chosen as an in vitro HF model, and were treated with galangin in different concentrations. Cell viability was analyzed using Cell Counting Kit-8 (CCK-8) and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, cell apoptosis was measured using flow cytometry, and the anti-fibrogenic effect of galangin was determined using quantitative reverse transcription polymerase chain reaction (RT-qPCR), immunofluorescence, and western blotting. The results show that the proliferation of LX-2 cells was efficiently inhibited by galangin, and apoptosis was induced in a dose-dependent manner. Both the mRNA and protein expression of α-SMA and collagen I were markedly downregulated. Galangin also inhibited the PI3K/Akt and Wnt/β-catenin signaling pathways and increased the Bax/Bcl-2 ratio. The results of this study suggest that galangin has an anti-fibrogenic effect and may represent a promising agent in the treatment of hepatic fibrosis.
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高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2021
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IF 4.36
Yang Wang,Shi-Yang Shen,Lei Liu,Xiao-Dong Zhang,Dan-Yang Liu,Na Liu,Bing-Hua Liu,Lei Shen
Ethnopharmacological relevance The diterpenoids extracted from Euphorbia kansui S.L. Liou ex S.B.Ho, Euphorbia fischeriana Steud. have good antitumor effects. Jolkinolide B has anti-breast cancer effect, but it is unclear whether it has different therapeutic effects between luminal A subtype and luminal B subtype breast cancer. Aim of the study This study investigated the Jolkinolide B has different therapeutic, important targets and pathways effects between luminal A subtype and luminal B subtype breast cancer. Materials and methods We used bioinformatics to predict the biological process and molecular mechanism of Jolkinolide B in treating two types of breast cancer. Then, in vitro, cultured MCF-7 cells and BT-474 cells were divided into control group, PI3K inhibitor + control group, Jolkinolide B group and PI3K inhibitor + Jolkinolide B group. The CCK-8 assay, Flow cytometric analysis and Transwell cell migration assay was used to detect the cell proliferation, apoptosis, and migration in each group, respectively. ELISA was used to measure the content of Akt and phosphorylated Akt (p-Akt) in cell lysis buffer. Results Compared to luminal A breast cancer, Jolkinolide B had more targets, proliferation, migration processes and KEGG pathways when treating luminal B subtype breast cancer. Jolkinolide B significantly prolonged the survival time of luminal B subtype breast cancer patients. Compared to the control group, the cell proliferation absorbance value (A value) and migration number of the two kinds of breast cancer cells in the Jolkinolide B group were decreased ( P < 0.01, n = 6), and the number of apoptotic cells was increased ( P < 0.01, n = 6). Compared to the Jolkinolide B group, the A value and migration number of the two types of breast cancer cells were significantly decreased in the PI3K inhibitor + Jolkinolide B group ( P < 0.01, n = 6), and the number of apoptotic cells was significantly increased ( P < 0.01, n = 6). In addition, compared to MCF-7 cells, the A value and migration number of BT-474 cells stimulated with Jolkinolide B were significantly decreased ( P < 0.01, n = 6), and the number of apoptotic cells was significantly increased ( P < 0.01, n = 6). Akt and p-Akt protein levels in the two breast cancer cell lines in the Jolkinolide B group were all decreased ( P < 0.01, n = 6), especially in BT-474 cells stimulated by Jolkinolide B. Conclusion Jolkinolide B regulates the luminal A and luminal B subtypes of breast cancer through PI3K-Akt, EGFR and other pathways. Jolkinolide B has more significant therapeutic effect on luminal B subtype breast cancer. In vitro, experiments verified that Jolkinolide B significantly inhibited the proliferation and migration activity of BT-474 breast cancer cells by downregulating the PI3K-Akt pathway.
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JOURNAL OF ETHNOPHARMACOLOGY
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2017
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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
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2024
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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 MOLECULAR SCIENCES
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2025
·Vol. 26
·期 5
·2118
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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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INTERNATIONAL IMMUNOPHARMACOLOGY
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2024
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IF 4.8
Jianfa Wu,Lingli Jiang,Sihong Wang,Lei Peng,Rong Zhang,Zhou Liu
The involvement of Interferon-stimulated exonuclease gene 20 (ISG20) has been reported in renal clear cell carcinoma, hepatocellular carcinoma, and cervical cancer. However, its role in ovarian cancer chemotherapy remains unclear. In this study, we conducted a comparative analysis of TGF-β1 and ISG20 in cisplatin-sensitive and cisplatin-resistant ovarian cancer cells and tissues using qRT-PCR and a tissue immunofluorescence analysis. We also investigated the impact of ISG20-targeted drugs (IFN-γ) and TGF-β1 inhibitors on cisplatin response both in vivo and in vitro. Additionally, we assessed the effects of TGF-β1 or ISG20 on the polarization of tumor-associated macrophages through flow cytometry and ELISA analysis. Our findings revealed that ISG20 expression was lower in cisplatin-resistant tissues compared to cisplatin-sensitive tissues; however, overexpression of ISG20 sensitized ovarian cancer to cisplatin treatment. Furthermore, activation of ISG20 expression with IFN-γ or TGF-β1 inhibitors enhanced the sensitivity of ovarian cancer cells to cisplatin therapy. Notably, our results demonstrated that TGF-β1 promoted M2-type macrophage polarization as well as PI3K/mTOR pathway activation by suppressing ISG20 expression both in vivo and in vitro. In conclusion, our study highlights the critical role played by ISG20 within the network underlying cisplatin resistance in ovarian cancer. Targeting ISG20 using IFN-γ or TGF-β1 inhibitors may represent a promising therapeutic strategy for treating ovarian cancer.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2025
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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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Cancer Cell International
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2021
·Vol. 21
·期 1
·1-15
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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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DRUG DEVELOPMENT RESEARCH
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2021
·Vol. 83
·期 1
·64-74
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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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Food Bioscience
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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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Chinese Journal of Natural Medicines
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2025
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IF 4.9
Yang Liu,Quanwei Sun,Xuefei Xu,Mengmeng Li,Wenheng Gao,Yunlong Li,Ye Yang,Dengke Yin
Ulcerative colitis (UC) is a chronic inflammatory disorder with a complex etiology, characterized by intestinal inflammation and barrier dysfunction. Platycodon grandiflorus polysaccharides (PGP), the primary component of Platycodon grandiflorus , and hesperidin (Hesp), a prominent active component in Citrus aurantium L. (CAL), have both demonstrated anti-inflammatory properties. This study aims to elucidate the underlying mechanism of the synergistic effect of PGP combined with Hesp on UC, focusing on the coordinated interaction between the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) and Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathways. A mouse model of UC induced by dextran sulfate sodium (DSS) and a cell model using lipopolysaccharide (LPS)-induced RAW264.7/IEC6 cells were employed to investigate the in vitro and in vivo anti-inflammatory effects of PGP combined with Hesp on UC and its potential mechanism of action. The results indicated that compared to the effects of either drug alone, the combination of PGP and Hesp significantly modulated inflammatory factor levels, inhibited oxidative stress, regulated colonic mucosal immunity, suppressed apoptosis, and restored intestinal barrier function in vitro and in vivo . Further in vitro studies revealed that PGP significantly inhibited the PI3K/AKT signaling pathway, while Hesp significantly inhibited the JAK2/STAT3 signaling pathway. The use of inhibitors and activators targeting both pathways validated the synergistic effects of PGP combined with Hesp on the PI3K/AKT and JAK2/STAT3 signaling pathways. These findings suggest that PGP combined with Hesp exhibits a synergistic effect on DSS-induced colitis, potentially mediated through the phosphatase and tensin homolog (PTEN)/PI3K/AKT and interleukin-6 (IL-6)/JAK2/STAT3 signaling pathways.
研究领域:
免疫学
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分子生物学
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药理学
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炎症性肠病研究
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信号转导
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BMC Pregnancy and Childbirth
·
2026
·Vol. 26
·期 1
·363
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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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