Aloe-emodin (AE) is the major bioactive component in aloe and known to exhibit anti-inflammatory activities. However, it has not been elucidated whether its anti-inflammatory potency can contribute to the elimination of obesity. The aim of the current study is to investigate the effect of AE on toll-like receptor 4 (TLR4) pathways in the presence of lipopolysaccharide (LPS) in 3T3-L1 adipocytes. 3T3-L1 adipocytes were treated with AE (0-20 μM) for one hour, followed by LPS treatment for 30 min and then, adipokine mRNA expression levels were measured. Next, TLR4-related molecules were measured in LPS-stimulated 3T3-L1 adipocytes. AE significantly decreased the mRNA expression of the tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1) in a dose-dependent manner. Moreover, AE suppressed TLR4 mRNA expression. Further study showed that AE could suppress the nuclear factor-κB (NF-κB) and phosphorylation of extracellular receptor-activated kinase (pERK). The results of this study suggest that AE directly inhibits TLR4/NF-κB/ERK signaling pathways and decreases the inflammatory response in adipocytes.

본 연구에서 상동나무 가지 추출물(STB-E100)은 대장암 세포에서 세포사멸을 유도하여 세포생육을 억제하였다. 또한 Iκ B-α 인산화를 통한 IκB-α 단백질 분해를 유도하며 이로 인해 P65 핵내 전이를 유도하여 NF-κB 신호전달을 활성화시킨다. NF-κB 신호전달 활성화는 GSK3β 활성화를 통해 P65 핵내 전 이를 유도에 의한 것이지만 IκB-α분해는 GSK3β 의존성이 아니다. 상동나무 가지 추출물은 이러한 신호전달 활성화를 통해 세포사멸을 유도하여 대장암의 세포생육을 억제한다. 본 결과를 바탕으로 상동나무 가지가 암 예방 및 치료를 목적으로한 표적 요법에서 항암제 개발의 잠재적 활용 소재로서 이용 가능하다고 사료된다. 그러나 대장암 세포에서 상동나무 가지 추출물에 의해 유도된 NF-κB 신호전달 작용기전을 좀 더 구체적으로 구명할 필요가 있고 대장암에 대한 세포사멸과 작용기전의 정확한 관련성을 조사하기 위해 추가적인 연구가 필요하다.

Long-term ultraviolet (UV) exposure accelerates the phenomenon of skin photo-aging by activating collagenase and elastase. In this study, we aimed to investigate the effects of a combination of grapefruit and rosemary extracts (cG&Re) on UVB-irradiated damage in HaCaT cells and dorsal mouse skin. In HaCaT cells, cG&Re recovered UVB-reduced cell viability and inhibited protein expression of mitogen-activated protein kinases (MAPKs), such as extracellular signal-regulated kinases (p-Erk), c-Jun N-terminal kinases (p-JNK), and a class of MAPKs (p-P38). Also, cG&Re suppressed UVB-induced collagen and elastin degradation by decreasing matrix metalloproteinases (MMPs) and nuclear factor kappa light chain enhancer of activated B cells (NF-κB) expression, which is a transcription factor. Similar results were observed in dorsal mouse skin. Taken together, our data indicate that cG&Re prevent UVB-induced skin photo-aging due to collagen/elastin degradation via activation of MAPKs, MMPs, and the NF-κB signaling pathway in vitro and in vivo.

Honey used as conventional medicine has various pharmacological properties. In the honey and anti-inflammatory effect, Gelam honey and Manuka honey has been reported to exert anti-inflammatory activity. However, the anti-inflammatory effect and potential mechanisms of acacia honey (AH) are not well understood. In this study, we investigated anti-inflammatory activity and mechanism of action of AH in LPS-stimulated RAW264.7 cells. AH attenuated NO production through inhibition of iNOS expression in LPS-stimulated RAW264.7 cells. AH also decreased the expressions of IL-1β, IL-6 and TNF-α as pro-inflammatory cytokines, and MCP-1 expression as a pro-inflammatory chemokine. In the elucidation of the molecular mechanisms, AH decreased LPS-mediated IκB-α degradation and subsequent nuclear accumulation of p65, which resulted in the inhibition of NF-κB activation in RAW264.7 cells. AH dose-dependently suppressed LPS-mediated phosphorylation of ERK1/2 and p38 in RAW264.7 cells. In addition, AH significantly inhibited ATF2 phosphorylation and nuclear accumulation of ATF2 in LPS-stimulated RAW264.7 cells. These results suggest that AH has an anti-inflammatory effect, inhibiting the production of pro-inflammatory mediators such as NO, iNOS, TNF-α, IL-6, IL-1β and MCP-1 via interruption of the NF-κB and MAPK/ATF2 signaling pathways.