Department of Prosthodontics, College & Affiliated Hospital of Stomatology, Guangxi Medical University, Nanning, Guangxi, China.
Guangxi Key Laboratory of Oral and Maxillofacial Restoration and Reconstruction, Guangxi Medical University, Nanning, Guangxi, China.
Immunol Invest. 2024 May;53(4):604-621. doi: 10.1080/08820139.2024.2321353. Epub 2024 Feb 28.
Mogroside V (MV) has anti-inflammatory properties. However, its impact on macrophage polarization under diabetic condition is yet unclear. This study aimed to investigate effects and underlying mechanisms of MV on inflammatory response and M1 polarization of bone marrow-derived macrophages (BMDMs) from diabetic mice.
BMDMs were isolated from normal and diabetic C57BL/6 mice. LPS and IFN-γwere used to produce M1-polarized BMDMs. MV treatment was administered throughout the M1 polarization process with or without SB203580 or PDTC. Surface markers CD11b, F4/80 and CD86 of macrophages were identified using flow cytometry or immunofluorescence staining. Inflammatory cytokines IL-1β and IL-6 and phosphorylation levels of p65 and p38 were examined by western blot.
High glucose increased proportion of CD11bF4/80CD86 cells, protein levels of inflammatory cytokines IL-1β and IL-6 and phosphorylation levels of p65 and p38 in LPS+IFN-γ-induced BMDMs, while they were decreased upon MV treatment. Additionally, these effects were further downregulated when MV was co-added with SB203580 or PDTC.
MV suppressed M1 macrophage polarization and inflammatory response, which was partially through NF-κB and p38 MAPK in LPS+IFN-γ induced BMDMs under high glucose condition, implying the potential of MV in treatment for inflammatory complications of diabetes.
罗汉果苷 V（MV）具有抗炎特性。然而，其在糖尿病条件下对巨噬细胞极化的影响尚不清楚。本研究旨在探讨 MV 对糖尿病小鼠骨髓来源的巨噬细胞（BMDM）炎症反应和 M1 极化的影响及其潜在机制。
从正常和糖尿病 C57BL/6 小鼠中分离 BMDM。用 LPS 和 IFN-γ诱导产生 M1 极化的 BMDM。MV 处理在 M1 极化过程中进行，或与 SB203580 或 PDTC 共同给药。通过流式细胞术或免疫荧光染色鉴定巨噬细胞的表面标志物 CD11b、F4/80 和 CD86。通过 Western blot 检测炎症细胞因子 IL-1β和 IL-6 以及 p65 和 p38 的磷酸化水平。
高葡萄糖增加了 LPS+IFN-γ诱导的 BMDM 中 CD11bF4/80CD86 细胞的比例、炎症细胞因子 IL-1β和 IL-6 的蛋白水平以及 p65 和 p38 的磷酸化水平，而 MV 处理则降低了这些水平。此外，当 MV 与 SB203580 或 PDTC 共同给药时，这些作用进一步下调。
MV 抑制了 M1 巨噬细胞极化和炎症反应，这部分是通过高葡萄糖条件下 LPS+IFN-γ诱导的 BMDM 中的 NF-κB 和 p38 MAPK 实现的，这暗示了 MV 在治疗糖尿病炎症并发症方面的潜力。
