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炎症细胞因子对人颗粒细胞中巨噬细胞集落刺激因子和单核细胞趋化蛋白-1分泌的影响。

The effect of inflammatory cytokines on secretion of macrophage colony-stimulating factor and monocyte chemoattractant protein-1 in human granulosa cells.

作者信息

Kawano Yasushi, Fukuda Junichiro, Itoh Hiroko, Takai Noriyuki, Nasu Kaei, Miyakawa Isao

机构信息

Department of Obstetrics and Gynecology, Faculty of Medicine, Oita University, Oita, Japan.

出版信息

Am J Reprod Immunol. 2004 Aug;52(2):124-8. doi: 10.1111/j.1600-0897.2004.00198.x.

Abstract

PROBLEM

In order to investigate the role of macrophage colony-stimulating factor (M-CSF) and monocyte chemoattractant protein -1 (MCP-1) in human ovulation, we studied the regulation of M-CSF and MCP-1 in cultured human granulosa cells.

METHOD OF STUDY

Immortalized granulosa cells (GC1a) were cultured in serum-free medium, and incubated with interleukin (IL)-1alpha, IL-1 receptor antagonist (ra) and tumor necrosis factor (TNF)-alpha. The supernatants were collected, and M-CSF and MCP-1 were measured by ELISA.

RESULTS

The levels of M-CSF and MCP-1 were increased after treatment with IL-1alpha (1 nm) and TNF-alpha (1 nm) in a time-dependent manner. The levels of M-CSF and MCP-1 were significantly increased after treatment with IL-1alpha and TNF-alpha in a dose-dependent manner. However, the levels of M-CSF and MCP-1 were significantly decreased by treatment with IL-1alpha (1 nm) and/or increasing concentrations of IL-1 ra.

CONCLUSIONS

Our data indicated that M-CSF and MCP-1 were regulated by IL-1alpha and TNF-alpha. It was suggested that M-CSF and MCP-1 may play an important role in human preovulatory processes.

摘要

问题

为了研究巨噬细胞集落刺激因子(M-CSF)和单核细胞趋化蛋白-1(MCP-1)在人类排卵中的作用,我们研究了培养的人颗粒细胞中M-CSF和MCP-1的调控情况。

研究方法

将永生化颗粒细胞(GC1a)在无血清培养基中培养,并用白细胞介素(IL)-1α、IL-1受体拮抗剂(ra)和肿瘤坏死因子(TNF)-α进行孵育。收集上清液,并用酶联免疫吸附测定法(ELISA)检测M-CSF和MCP-1。

结果

用IL-1α(1纳米)和TNF-α(1纳米)处理后,M-CSF和MCP-1的水平呈时间依赖性增加。用IL-1α和TNF-α处理后,M-CSF和MCP-1的水平呈剂量依赖性显著增加。然而,用IL-1α(1纳米)和/或增加浓度的IL-1 ra处理后,M-CSF和MCP-1的水平显著降低。

结论

我们的数据表明,M-CSF和MCP-1受IL-1α和TNF-α调控。提示M-CSF和MCP-1可能在人类排卵前过程中起重要作用。

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