[논문]금화규(Abelmoschus manihot) 뿌리 추출물의 면역증진 및 항비만효과

유주형; 금나경; 여주호; 정진부

doi:10.7732/kjpr.2021.34.5.411

금화규(Abelmoschus manihot) 뿌리 추출물의 면역증진 및 항비만효과
Immuno-enhancing and Anti-obesity Effect of Abelmoschus manihot Root Extracts 원문보기

韓國資源植物學會誌 = Korean journal of plant resources, v.34 no.5, 2021년, pp.411 - 419

유주형 (국립안동대학교 생약자원학과) , 금나경 (국립안동대학교 생약자원학과) , 여주호 (국립안동대학교 생약자원학과) , 정진부 (국립안동대학교 생약자원학과)

초록
AI-Helper

본 연구에서 금화규 뿌리 추출물(AMR)이 마우스 대식세포인 RAW264.7 세포의 활성화 유도를 통한 면역증진 활성과 마우스 지방전구세포인 3T3-L1 세포의 지질축적억제를 통한 항비만 활성을 평가하였다. 금화규 뿌리 추출물(AMR)은 전반적으로 RAW264.7 세포에서 TLR2/TLR4의 자극을 통해 p38과 JNK를 활성화시켜 NO, iNOS, IL-1𝛽, IL-6, TNF-𝛼와 같은 면역증진 인자의 발현을 증가시키는 것으로 판단된다. 그러나 IL-6의 경우, p38과 JNK 활성화에 의존하지 않는 것으로 확인되어 TLR2/4에 의한 다른 신호전달이 관여하는 것으로 사료되어 추가적인 연구가 필요하다. 또한, 금화규 뿌리 추출물(AMR)은 PPAR𝛾의 과대발현을 억제하여 지방전구세포의 성숙한 지방세포로의 분화를 억제하고, 성숙한 지방세포에서 CEBP𝛼, PPAR𝛾, perilipin-1, FABP4, adiponectin의 발현을 억제하여 지방세포 내 지질 형성 및 축적을 억제하는 것으로 판단된다. 본 연구를 통해 구명된 결과들은 금화규 뿌리 추출물(AMR)이 향후 면역증진 및 항비만을 위한 보조제 또는 건강 기능성 식품과 의약품으로의 개발 및 활용이 가능할 것으로 생각된다.

Abstract ▼ AI-Helper

In this study, we investigated in vitro immune-enhancing and anti-obesity activity of Abelmoschus manihot roots (AMR) in mouse macrophage RAW264.7 cells and mouse adipocytes 3T3-L1 cells. AMR increased the production of immunostimulatory factors such as nitric oxide (NO), inducible nitric oxide synthase (iNOS), interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in RAW264.7 cells. The inhibition of toll like receptor (TLR) 2 and 4 blocked AMR-mediated production of immunostimulatory factors in RAW264.7 cells. In addition, the inhibition of mitogen-activated protein kinases (MAPKs) signaling pathway reduced AMR-mediated production of immunostimulatory factors. From these results, AMR is considered to have immune-enhancing activity through TLR2/4-mediated activation of MAPKs signaling pathway. In addition, AMR inhibited lipid accumulation and reduced the protein level such as CCAAT enhancer-binding protein alpha (CEBPα), peroxisome proliferator-activated receptor gamma (PPARγ), perilipin-1, adiponectin and fatty acid binding protein 4 (FABP4) associated with lipid accumulation in 3T3-L1 cells, indicating that AMR may have anti-obesity activity. Based on these results, AMR is expected to be used as a potential functional agent for immune enhancement and anti-obesity.

주제어

표/그림 (7)

표 Table 1. Sequence of oligonucleotide primers used for RT-PCR
그림 Fig. 1. Effect of AMR on macrophage activation in RAW264.7 cells. RAW264.7 cells were treated with AMR for 24 h. NO level (A), mRNA level (B). GAPDH was used as internal control for RT-PCR.
그림 Fig. 2. Effect of TLR2 and TLR4 on the production of immune enhancing factors in AMR-treated RAW264.7 cells. RAW264.7 cells were pretreated with C29 (TLR2 inhibitor, 100 μM) or TAK-242 (TLR4 inhibitor, 5 μM) for 2 h and co-treated with AMR (50 ㎍/mL) for 24 h. NO level (A) and mRNA level (B) were measured by Griess assay and RT-PCR, respectively. *P < 0.05 compared to the cells without the treatment. #P < 0.05 compared to the cells treated with AMR alone. GAPDH was used as internal control for RT-PCR.
그림 Fig 3. Effect of MAPK signaling pathway on the production of immune enhancing factors in AMR-treated RAW264.7 cells. RAW264.7 cells were pretreated with PD98059 (ERK1/2 inhibitor, 40 μM), SB203580 (p38 inhibitor, 40 μM), SP600125 (JNK inhibitor, 40 μM) for 2 h and then co-treated with AMR for 24 h. NO level (A) and mRNA level (B) were measured by Griess assay and RT-PCR. (C) RAW264.7 cells were treated with AMR for the indicated times. (D) RAW264.7 cells were pretreated with C29 (TLR2 inhibitor, 100 μM) or TAK-242 (TLR4 inhibitor, 5 μM) for 2 h and treated with AMR for 1 h. *P < 0.05 compared to the cells without the treatment. #P < 0.05 compared to the cells with AMR alone. GAPDH and Actin were used as internal control for RT-PCR and Western blot.
그림 Fig. 4. The effect of AMR on lipid accumulation in 3T3-L1 cells. 3T3-L1 cells were co-treated with DMI/insulin and AMR. *P < 0.05 compared to the cells without the treatment. #P < 0.05 compared to the cells treated with DMI/insulin alone. Actin was used as internal control for Western blot.
그림 Fig. 5. The effect of AMR on lipid accumulation in 3T3-L1 cells. 3T3-L1 cells were co-treated with DMI/insulin and AMR for indicated times. *P < 0.05 compared to the cells without the treatment. Actin was used as internal control for Western blot.
그림 Fig. 6. The effect of AMR on Inhibition of adipocyte differentitaion in 3T3-L1 cells. 3T3-L1 cells were co-treated with DMI and AMR for 48 h. Actin was used as internal control for Western blot.

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