[논문]작약(Paeonia lactiflora) 뿌리 추출물의 대식세포에서 p62/SQSTM1 증가를 통한 자가포식 유도

정진부

doi:10.7732/kjpr.2023.36.4.275

[국내논문] 작약(Paeonia lactiflora) 뿌리 추출물의 대식세포에서 p62/SQSTM1 증가를 통한 자가포식 유도
Induction of Autophagy by Paeonia lactiflora Root Extracts through Upregulation p62/SQSTM1 in RAW264.7 Cells 원문보기

韓國資源植物學會誌 = Korean journal of plant resources, v.36 no.4, 2023년, pp.275 - 281

초록
AI-Helper

본 연구에서 우리는 작약 뿌리 추출물이 TLR4/PI3K/Nrf2 신호전달을 통해 p62/SQSTM1을 증가시켜 대식세포에서 자가포식을 유도한다는 것을 확인하였다. 대식세포의 자가포식 유도는 선천성과 적응성 면역 반응 간의 연결을 강화해 백신 보조제 개발에 있어서 중요한 표적으로 사용되기 때문에, 작약 뿌리 추출물은 백신개발에 필수적인 백신보조제로의 활용이 가능할 것으로 생각된다.

Abstract ▼ AI-Helper

Autophagy contributes to enhancing the immune system (innate and adaptive immune system) against foreign pathogens. Autophagy of macrophages is used as a major indicator for developing vaccine adjuvants to increase the adaptive immune response. In this study, PLR activated autophagy and increased p62/SQSTM1. The knockdown of p62/SQSTM1 attenuated PLR-mediated autophagy. Inhibition of TLR4 blocked PLR-mediated increase in p62/SQSTM1 level and autophagy induction. In addition, inhibition of PI3K blocked HSL-mediated increase of p62/SQSTM1. PLR increased Nrf2 level and the inhibition of TLR4 and PI3K reduced PLR-mediated increase of Nrf2. Taken together, it is believed that PLR may induce autophagy through upregulating p62/SQSTM1 via TLR4/PI3K/Nrf2 signaling pathway.

Keyword

표/그림 (4)

그림 Fig. 1. Effect of PLR on autophagy induction and p62/SQSTM1 level in RAW264.7 cells. (A) RAW264.7 cells were treated with PLR for 24 h. Autophagy induction was measured using Autophagy Assay Kit. (B) RAW264.7 cells were treated with PLR for 24 h. p62/SQSTM1 level was measured using Western blot analysis. (C) RAW264.7 cells were treated with PLR (50 ㎍/mL) for the indicatd times. p62/SQSTM1 level was measured using Western blot analysis. (D) RAW264.7 cells were transfected with controlor p62/SQSTM1 siRNA for 48 h, and then treated with PLR (50 ㎍/mL) for 24 h. Autophagy induction was measured using Autophagy Assay Kit.
그림 Fig. 2. Effect of TLR2/4 on PLR-mediated increase in p62/ SQSTM1 and autophagy induction. (A) RAW264.7 cells were pre-treated with C29 (100 nM) or TAK-242 (10 ㎍/mL) for 2 h and then co-treated with PLR (50 ㎍/mL) for 6 h. p62/SQSTM1 level was measured using Western blot analysis. (B) RAW264.7 cells were pre-treated with C29 (100 nM) or TAK-242 (10 ㎍ /mL) for 2 h and then co-treated with PLR (50 ㎍/mL) for 24 h. Autophagy induction was measured using Autophagy Assay Kit.
그림 Fig. 3. Effect of kinases on PLR-mediated increase in p62/SQSTM1. (A) RAW264.7 cells were pre-treated with PD98059 (40 μM), SB203580 (40 μM), SP600125 (40 μM), BAY 11-7082 (BAY, 20 μM) or LY294002 (40 μM) for 2 h and then co-treated with PLR (50 ㎍/mL) for 6 h. p62/SQSTM1 level was measured using Western blot analysis. (B) RAW264.7 cells were treated with PLR (50 ㎍/mL) for the indicated times. p-PI3K and PI3K levels were measured using Western blot analysis. (C) RAW264.7 cells were pre-treated with TAK-242 (10 ㎍/mL) for 2 h and then co-treated with PLR (50 ㎍/mL) for 1 h. p-PI3K level was measured using Western blot analysis.
그림 Fig. 3. Effect of Nrf2 on PLR-mediated increase in p62/SQSTM1. (A) RAW264.7 cells were treated with PLR (50 ㎍/mL) for the indicated times. Nrf2 level was measured using Western blot analysis. (B) RAW264.7 cells were pre-treated with TAK-242 (10 ㎍ /mL) or LY294002 (40 μM) for 2 h and then co-treated with PLR (50 ㎍/mL) for 1 h. Nrf2 level was measured using Western blot analysis.

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