Abstract

Obesity is a major disease that causes significant complications. Inhibition of preadipocyte proliferation has the potential to prevent obesity and metabolic diseases. Melatonin is a pineal gland hormone that has various effects on cells and tissues. In this research, we investigated whether melatonin induces apoptosis in 3T3-L1 preadipocytes. 3T3-L1 preadipocytes were cultured until confluence and then treated with 0, 10, 100, and 1000 μM melatonin for 1, 3, and 5 days. A cell viability assay kit was used for determining cell viability. Cell death marker proteins were assessed by Western blot analysis using GAPDH for control. Apoptotic morphological changes with nuclei fragmentation were observed using DAPI staining. Melatonin treatment decreased the phosphorylated extracellular signal-regulated kinases (p-ERK) activation while increasing the activation of caspase-3, 8, and 9. Furthermore, melatonin not only increased Bcl-2-associated X protein (Bax) but decreased B-cell lymphoma 2 (Bcl-2) expression as dose increases from 0 to 1000 µM. The melatonin treatment also suppressed the growth of preadipocytes with increasing concentration. These effects were attenuated by luzindole, a melatonin receptor antagonist and U0126, an inhibitor of p-ERK activation. In conclusion, melatonin can induce apoptosis of 3T3-L1 preadipocytes via p-ERK decrease.

中文翻译：

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褪黑素诱导3T3-L1前脂肪细胞凋亡细胞死亡。

摘要

肥胖是引起重大并发症的主要疾病。抑制前脂肪细胞增殖具有预防肥胖和代谢疾病的潜力。褪黑激素是一种松果体激素，对细胞和组织具有多种作用。在这项研究中，我们调查了褪黑激素是否诱导3T3-L1前脂肪细胞凋亡。培养3T3-L1前脂肪细胞直至融合，然后分别用0、10、100和1000μM褪黑素处理1、3和5天。细胞活力测定试剂盒用于确定细胞活力。使用GAPDH作为对照，通过蛋白质印迹分析评估细胞死亡标记蛋白。使用DAPI染色观察到随着细胞核碎片的凋亡形态学变化。褪黑素处理减少了磷酸化的细胞外信号调节激酶（p-ERK）的激活，同时增加了caspase-3、8和9的激活。此外，褪黑素不仅增加了Bcl-2相关X蛋白（Bax），而且降低了B-细胞淋巴瘤2（Bcl-2）的表达随剂量从0增加到1000 µM。褪黑素处理还随着浓度的增加而抑制了前脂肪细胞的生长。褪黑激素受体拮抗剂luzindole和p-ERK激活抑制剂U0126减弱了这些作用。总之，褪黑激素可以通过减少p-ERK诱导3T3-L1前脂肪细胞凋亡。褪黑素处理还随着浓度的增加而抑制了前脂肪细胞的生长。褪黑激素受体拮抗剂luzindole和p-ERK激活抑制剂U0126减弱了这些作用。总之，褪黑激素可以通过减少p-ERK诱导3T3-L1前脂肪细胞凋亡。褪黑素处理还随着浓度的增加而抑制了前脂肪细胞的生长。褪黑激素受体拮抗剂luzindole和p-ERK激活抑制剂U0126减弱了这些作用。总之，褪黑激素可以通过减少p-ERK诱导3T3-L1前脂肪细胞凋亡。