a-MSH (α-Melanocyte-Stimulating Hormone), amide engages the melanocortin-1 receptor and activates cyclic AMP (cAMP) signaling via a G-protein transporter, can synthesize melanin. It is an endogenous neuropeptide, a post-translational derivative of pro-opiomelanocortin (POMC). It is an endogenous melanocortin receptor 4 (MC4R) agonist with anti-inflammatory and antipyretic activities[1-4,10].
α-MSH-treated(1 hour; 300pg/ml) T cells showed higher levels of protein ubiquitination. Resting T cells treated with alpha-MSH also demonstrated enhanced protein ubiquitination[5].In α-MSH-stimulated(1 µM, 72 h) B16F10 cells, autophagosomes engulfing melanosomes following Pt treatment[6]. α-MSH regulates central nervous system inflammation by acting directly on melanocortin receptors in glial cells. α-MSH regulates the activation of NFκB. α-MSH inhibits nuclear transmigration of transcription factor κB[7].
α-MSH(0.5mg/kg;i.p;28days) modulated the excitatory-inhibitory balance in the brain by restoring GABAergic inhibition and improved cognition in TgCRND8 mice[8]. α-MSH(2, 6, 20 or 60 nmol)plays an important regulatory role in the spinal defecation center of rats. Intrathecal administration of α-MSH in mice can enhance the colonic movement of the L6-S1 spinal cord and block the pelvic nerve, but the pro-kinetic effect of α-MSH disappeared[9].
References:
[1]. Kim MS, Rossi M, et,al.Hypothalamic localization of the feeding effect of agouti-related peptide and alpha-melanocyte-stimulating hormone. Diabetes. 2000 Feb;49(2):177-82. doi: 10.2337/diabetes.49.2.177. PMID: 10868932.
[2]. Singh M, Mukhopadhyay K. C-terminal amino acids of alpha-melanocyte-stimulating hormone are requisite for its antibacterial activity against Staphylococcus aureus. Antimicrob Agents Chemother. 2011 May;55(5):1920-9. doi: 10.1128/AAC.00957-10. Epub 2011 Jan 31. PMID: 21282427; PMCID: PMC3088230.
[3]. Catania A, Delgado R, et,al.alpha-MSH in systemic inflammation. Central and peripheral actions. Ann N Y Acad Sci. 1999 Oct 20;885:183-7. doi: 10.1111/j.1749-6632.1999.tb08675.x. PMID: 10816651.
[4]. Anderson EJ, Çakir I, et,al.60 YEARS OF POMC: Regulation of feeding and energy homeostasis by α-MSH. J Mol Endocrinol. 2016 May;56(4):T157-74. doi: 10.1530/JME-16-0014. Epub 2016 Mar 3. PMID: 26939593; PMCID: PMC5027135.
[5]. Biros DJ, Namba K, et,al.Alpha-MSH regulates protein ubiquitination in T cells. Cell Mol Biol (Noisy-le-grand). 2006 May 30;52(2):33-8. PMID: 16914084; PMCID: PMC4698146.
[6]. Hseu YC, Vudhya Gowrisankar Y, et,al. The in vitro and in vivo depigmenting activity of pterostilbene through induction of autophagy in melanocytes and inhibition of UVA-irradiated α-MSH in keratinocytes via Nrf2-mediated antioxidant pathways. Redox Biol. 2021 Aug;44:102007. doi: 10.1016/j.redox.2021.102007. Epub 2021 May 19. PMID: 34049220; PMCID: PMC8167190.
[7]. Lipton JM, Zhao H, et,al.Mechanisms of antiinflammatory action of alpha-MSH peptides. In vivo and in vitro evidence. Ann N Y Acad Sci. 1999 Oct 20;885:173-82. doi: 10.1111/j.1749-6632.1999.tb08674.x. PMID: 10816650.
[8]. Biros DJ, Namba K, et,al.Alpha-MSH regulates protein ubiquitination in T cells. Cell Mol Biol (Noisy-le-grand). 2006 May 30;52(2):33-8. PMID: 16914084; PMCID: PMC4698146.
[9].Ueda HH, Naitou K, et,al. α-MSH-induced activation of spinal MC1R but not MC4R enhances colorectal motility in anaesthetised rats. Sci Rep. 2021 Jan 12;11(1):487. doi: 10.1038/s41598-020-80020-x. PMID: 33436759; PMCID: PMC7803980.
[10].Song, X.; Mosby, N.; Yang, J.; Xu, A.; Abdel-Malek, Z.; Kadekaro, A.L. alpha-MSH activates immediate defense responses to UV-induced oxidative stress in human melanocytes. Pigment Cell Melanoma Res. 2009, 22, 809-818.
a-MSH(α-黑素细胞刺激素)通过G蛋白转运体与黑色素皮质素-1受体结合并激活环磷酸腺苷(cAMP)信号通路,可以合成黑色素。它是内源性神经肽,是促阿皮黑色素皮质素(POMC)的翻译后衍生物。它是内源性黑色素皮质素受体4(MC4R)激动剂,具有抗炎和退热活性[1-4,10]。
α-MSH-treated(1 hour; 300pg/ml) T细胞显示更高水平的蛋白泛素化。α-MSH处理的静止T细胞也表现出增强的蛋白泛素化[5]。在α-MSH刺激(1 µM, 72 h)的B16F10细胞中,Pt处理后自噬体吞噬黑素体[6]。α-MSH通过直接作用于神经胶质细胞的黑素皮质素受体调节中枢神经系统炎症。α-MSH调节NFκB的活化。α-MSH抑制转录因子κB的核迁移[7]。
α-MSH(0.5mg/kg;i.p;28d)通过恢复TgCRND8小鼠中的GABAergic抑制和改善认知来调节大脑兴奋-抑制平衡[8]。α-MSH(2、6、20、60 nmol)在大鼠脊柱排便中枢中起重要的调节作用。小鼠鞘内给予α-MSH可增强L6-S1脊髓的结肠运动,阻断盆腔神经,但α-MSH的促动力学作用消失[9]。
















