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  • Apigenin trihydroxyflavone a natural plant flavone is a

    2022-09-24

    Apigenin (4′, 5, 7-trihydroxyflavone), a natural plant flavone, is a bioactive compound present in a variety of fruits, vegetables, and medicinal plants, and its various beneficial biological activities have been reviewed (Zhou et al., 2017), including HIF-1α inhibition-mediated anti-tumor. Recently, our study found that apigenin could improve the abnormal myocardial glucolipid metabolism and down-regulate the myocardial HIF-1α protein expression in renovascular hypertension-induced cardiac hypertrophic rats (Zhu et al., 2016). However, whether or not the ameliorative effect of glucolipid metabolism is from the reduction of HIF-1α expression remains uncertain. The aim of our present study was to examine the exact relationship between them in angiotensin Ⅱ (Ang Ⅱ)/hypoxia-induced hypertrophic H9c2 Regorafenib and HIF-1α overexpression H9c2 cells in vitro.
    Materials and methods
    Results and discussion
    Conclusion The present results, in accordance with our previous results of renovascular hypertensive cardiac hypertrophy (Zhu et al., 2016), demonstrated that apigenin could exert a beneficial ameliorative effect on abnormal glucolipid metabolism in AngⅡ/hypoxia-stimulated or LV-HIF-1α-transfected H9c2 cells, and its mechanisms were associated with the inhibition of HIF-1α expression and subsequent upregulation of PPARα-mediated CPT-1 and PDK-4 expressions and downregulation of PPARγ-mediated GPAT and GLUT-4 expressions. These findings provide a novel potential application of apigenin in the prevention and treatment of cardiovascular diseases.
    Conflict of interest
    Acknowledgments This work was supported by a grant from the Postgraduate Innovative Foundation of Jiangsu Province (No. KYLX15-1208), China.
    Introduction As the unique somatic cells within the seminiferous tubules, Sertoli cells play essential roles in regulating normal spermatogenesis. The number of Sertoli cells in the adult testis determines both testis size and daily sperm production. This relationship occurs because each Sertoli cell has a fixed capacity for the number of germ cells that it can support [1]. In rodents, Sertoli cells proliferate during fetal and neonatal life up to 15 days of age. Around 15–18 days of age the blood-testis barrier is formed and Sertoli cells keep on maturating to attain the ability to sustain full spermatogenesis. In addition to the master role of FSH, Sertoli cell proliferation and maturation are regulated by a number of hormonal cues, which include among others, thyroid hormone, retinoic acid, activin, and testosterone [2]. FSH actions can be demonstrated during fetal and the whole postnatal life. FSH regulates Sertoli cell proliferation during fetal and early postnatal life and its maturation after cessation of mitosis at puberty [3]. The molecular mechanisms underlying FSH action on Sertoli cell proliferation have not been fully elucidated yet. In this respect, there are scarce studies which analyze FSH-activated transcription factors involved in Sertoli cell proliferation. Within these studies, the participation of c-Myc in the regulation of Sertoli cell proliferation by FSH has been demonstrated [4]. The heterodimeric hypoxia-inducible factors (HIFs) are critical transcriptional regulators of cell physiology. HIFs consist of an α subunit (HIF-1α, HIF-2α or HIF-3α) and a β subunit (HIF-β) [5]. While HIF-β is expressed constitutively, HIF-α levels are regulated by hypoxia and by different hormones under normoxic conditions. Consequently, HIF activity is regulated through the amount of α subunit in the cell. HIF-1α and HIF-2α are closely related and their interaction with HIF-β subunit result in HIF-1 and HIF-2, respectively. Both active transcription factors bind to hypoxia-response elements (HRE) and stimulate target genes such as those related to angiogenesis, energy metabolism, cell growth and cell cycle progression [6]. HIF-3α is the most distantly related subunit in its primary structure and the active transcription factor HIF-3 functional role still has to be elucidated.