FABPH_BOVIN H-FABP ELISA tesk kit
- Known as:
- FABPH_BOVIN H-FABP Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen16024
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- FABPH_BOVIN H-FABP ELISA tesk kit
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- Phenotypic switching of vascular smooth muscle cells (VSMCs), leading to neointima formation, is a main cause of in-stent restenosis after coronary stent implantation, resulting in poor patient prognosis. Inhibition of VSMC proliferation, migration, and synthetic phenotype transition holds promise for preventing and treating neointimal hyperplasia and restenosis. GW0742, a peroxisome proliferator-activated receptor (PPAR)-β/δ agonist, has been reported to suppress atherosclerosis and myocardial ischemia-reperfusion injury. However, its role in neointima formation has not been previously studied. In this study, we found that GW0742 significantly inhibited carotid artery injury-induced neointimal hyperplasia in mice. In vitro experiments including cell counting, EdU staining, and proliferation marker detection revealed that GW0742 markedly suppressed Platelet-derived growth factor-BB (PDGF-BB)-induced proliferation of human aortic smooth muscle cells (HASMCs). Flow cytometry analysis showed that GW0742 treatment arrested cells in the G2/M phase. Transwell assays demonstrated that GW0742 inhibited HASMCs migration. Moreover, GW0742 reduced the expression of migration-associated proteins matrix metalloproteinases 2 (MMP2) and matrix metalloproteinases 9 (MMP9), while increasing contractile markers alpha-smooth muscle actin (α-SMA) and calponin 1 (CNN1), suggesting that GW0742 suppresses HASMC proliferation, migration, and phenotypic switching, thereby preserving the contractile phenotype. RNA sequencing revealed that GW0742 regulates fatty acid metabolism by upregulating fatty acid binding protein 3 (FABP3) expression to counteract PDGF-BB-induced VSMC phenotypic switching. Knockdown of FABP3 significantly abrogated the inhibitory effects of GW0742 on VSMC proliferation, migration, and synthetic phenotype transition. Taken together, our findings demonstrate that GW0742 upregulates FABP3 expression, leading to the inhibition of VSMC proliferation, migration, and phenotypic switching, and ultimately suppressing neointima formation. These results underscore the therapeutic potential of GW0742 for the prevention and treatment of vascular restenosis. - Source: PubMed
Publication date: 2026/08/12
Wang XueshengChen JingjieHuo BoWu XingliangLin WenxinJiang Ding-ShengZhang Yu-SongFeng XinGong Fu-Han - Perfluorooctanoic acid (PFOA) exposure has been associated with various negative effects on the cardiovascular system, including myocardial infarction. During myocardial infarction, ischemia-reperfusion (IR) injury is an important event, significantly affecting prognosis, while the effects of PFOA exposure on IR injury were not previously investigated. In the current study, C57B6 mice were pre-exposed to 0.005, 0.05 or 0.5 mg/kg/day PFOA for four weeks, and then IR injury was achieved with left anterior descending coronary artery ligation. The severity of IR injury was assessed with echocardiography, 2,3,5-triphenyltetrazolium chloride (TTC) staining, hematoxylin & eosin staining and Masson trichrome staining, along with serum biomarkers for myocardial injury and oxidative stress. To investigate the molecular mechanism, peroxisome proliferation activated receptor alpha (PPAR alpha) antagonist GW6471 was co-administered with PFOA, and animals were subjected to identical morphological, functional and biochemical evaluations. qRT-PCR and western blotting were utilized to assess PPAR alpha downstream genes: carnitine palmitoyl transferase 1b (CPT1b) and fatty acid binding protein 3 (FABP3) in heart tissue samples. The results indicated that pre-exposure to 0.05 or 0.5 mg/kg PFOA for 4 weeks significantly increased the severity of IR injury as indicated by morphological, functional and biochemical parameters, while co-administration of GW6471 alleviated such effects. Pre-exposure to PFOA significantly elevated the expression of CPT1b and FABP3 in myocardial tissues, whose extent corresponded to the severity of IR injury well. Meanwhile, co-exposure to GW6471 effectively alleviated such changes, suggesting that activation of PPAR alpha related fatty acid metabolism is likely involved in PFOA-mediated exacerbation of IR injury. - Source: PubMed
Publication date: 2026/08/03
Chen ChenBu FangfangGao YaWang YilinZhang HanyueGao JiaqiYuan JiashuoWang ZhongyuZhong YuxuJiang QixiaoShu XinYuan Junhua - Long distance migration in birds requires dynamic remodelling of flight muscle induced by behavioural, endocrine and metabolic adjustments. Here, we studied redheaded buntings in the nonmigratory and migratory state to assess changes in plasma hormones, muscle fibre diameter, lipid droplet accumulation and gene expression in the pectoralis and supracoracoideus muscles. We investigated genes that are involved in (1) muscle growth and atrophy, and (2) fatty acid transport and metabolism. Long-day exposure induced nighttime migratory restlessness, increased body mass, fat and muscle scores, and enlarged testes, compared with short days. Plasma insulin and testosterone levels were elevated in the migratory group, whereas T3 levels remained unchanged. Only the pectoralis muscle showed significant hypertrophy and high lipid accumulation under long days, whereas the supracoracoideus remained unchanged. We found elevated mRNA levels of fabp3 (fatty acid binding protein) and ar (androgen receptors) in both muscles, but scd1 (stearoyl-coA desaturase 1) only in the pectoralis. In contrast, igf1 (insulin-like growth factor 1) mRNA levels decreased in pectoral muscle in migratory state. These findings suggest that although fabp3 may facilitate fatty acid transport to both muscles, scd1 contributes to lipogenesis in pectoral muscle only. This suggests that pectoral muscles play a more active role than supracoracoideus muscle in uptake, modification and storage of lipids during migration. These findings demonstrate muscle-specific physiological remodelling underlying the migratory phenotype in buntings. Network analysis further revealed greater integration of phenotype, histology, hormone and molecular traits during migration, suggesting enhanced coordination of physiological systems during migration. - Source: PubMed
Publication date: 2026/08/21
Yadav VibhaSharma AakanshaTiwari JyotiRani SangeetaMalik Shalie - This study investigated the impact of dietary alginate oligosaccharides (AOS) on the meat quality of breast muscle in broilers exposed to heat stress (HS). In broilers exposed to HS, dietary AOS enhanced pH and the activities of catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione S-transferase (GST) (P < 0.05), while decreasing drip loss and malondialdehyde (MDA) concentration in breast muscle (P < 0.05). Non-targeted metabolomics analysis revealed that AOS regulates lipid metabolism of breast muscle. Furthermore, AOS upregulated the expression of antioxidant genes GSTA3, GPX3, CAT1, NQO1, and muscle fiber transformation regulators MyH1D, PGC-1α, MEF2C (P < 0.05), while downregulating lipogenic genes SREBP-1, ACC, FAS and FABP3, and the fast muscle marker MyH9 (P < 0.05). Concomitantly, AOS enhanced the phosphorylation modification level of Nrf2 and AMPK proteins (P < 0.05). Therefore, AOS improves the meat quality of breast muscle in broilers exposed to HS by improving the oxidative stability, promoting the transformation of fast muscle fibers into slow muscle fibers, and alleviating lipid metabolism disorders. - Source: PubMed
Publication date: 2026/07/17
Yao Qing-HuaWang Yao-YaoYe Xue-QingZhao Zhong-XiangLiu Hui-MeiLiu Wen-Chao - To investigate the effect and underlying mechanism of securinine (Sec) in ovarian cancer (OC) based on network pharmacology, in vivo experiments and proteomics. - Source: PubMed
Publication date: 2026/07/15
Tu Xin-MinZhang Ya-JuanMiao Cheng-YuKang JieShi Yu-HengWang Chen-LinHan BingKai Guo-Yin