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프라모더 바하더 케이씨,강봉석,정남호 한국생명과학회 2021 생명과학회지 Vol.31 No.5
Inflammation induced by metabolic syndromes, cancers, injuries, and sepsis can alter cellular metabolism by reducing mitochondrial function via oxidative stress, thereby resulting in neuropathy and muscle atrophy. In this study, we investigated whether butyrate, a short chain fatty acid produced by gut microbiota, could prevent mitochondrial dysfunction and muscle atrophy induced by lipopolysaccharide (LPS) in the C2C12 cell line. LPS-activated MAPK signaling pathways increased the levels of the mitochondrial fission signal, p-DRP1 (Ser616), and the muscle atrophy marker, atrogin 1. Interestingly, butyrate significantly inhibited the phosphorylation of JNK and p38 and reduced the atrogin 1 level in LPS-treated C2C12 cells while increasing the phosphorylation of DRP1 (Ser637) and levels of mitofusin2, which are both mitochondrial fusion markers. Next, we investigated the effect of MAPK inhibitors, finding that butyrate had the same effect as JNK inhibition in C2C12 cells. Also, butyrate inhibited the LPS-induced expression of pyruvate dehydrogenase kinase 4 (PDK4), resulting in decreased PDHE1α phosphorylation and lactate production, suggesting that butyrate shifted glucose metabolism from aerobic glycolysis to oxidative phosphorylation. Finally, we found that these effects of butyrate on LPS-induced mitochondrial dysfunction were caused by its antioxidant effects. Thus, our findings demonstrate that butyrate prevents LPS-induced muscle atrophy by improving mitochondrial dynamics and metabolic stress via the inhibition of JNK phosphorylation. Consequently, butyrate could be used to improve LPS-induced mitochondrial dysfunction and myopathy in sepsis.
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Yam Bahadur KC(얌 바하더 케이씨),Sunil Poudel(수닐 포우델),Eon Ju Jeon(전언주),Ho Sang Shon(손호상),Sung June Byun(변승준),Nam Ho Jeoung(정남호) 한국생명과학회 2018 생명과학회지 Vol.28 No.12
Warburg 효과의 발생은 고형암에서 화학적 항암제의 내성을 발생시킨다. 따라서 호기성 해당과정과 같은 에너지 대사과정은 암 치료의 중요한 표적으로 알려져 있다. Pyruvate dehydrogenase kinase (PDK) 활성 억제물질로 알려진 dichloroacetate (DCA)는 많은 암세포에서 포도당의 호기성 해당과정을 산화적인산화 과정으로 전환시킬 수 있음이 보고되었다. 이 연구는 치료가 매우 어렵다고 알려진 인간 역분화 갑상선 암세포주인 8505C의 성장에 미치는 DCA효과를 조사하였다. DCA는 정상 갑상선 세포주의 성장에는 영향을 주지 않은 반면 8505C 세포주의 성장을 특이적으로 저해하였다. DCA의 처리에 의해 8505C 세포주는 HIF1α, PDK1, Bcl-2와 같은 항-세포자살 관련 단백질들의 발현이 감소하고, Bax와 p21과 같은 세포자살 유도 단백질과 세포주기 억제 단백질의 증가로 인하여 세포주기 정지와 세포자살 유도에 의해 성장이 억제되었다. 이런 세포의 변화는 DCA 처리에 의한 활성산소족의 생산이 증가하고, 포도당 대사가 호기성 해당과정에서 산화적인산화 과정으로 전환되었기 때문이란 것을 확인하였다. 흥미롭게도, DCA는 포도당 대사과정의 변화뿐만 아니라 sodium/iodine symporter (NIS)의 발현양도 증가시킨다는 것을 확인하였다. 이 연구의 결과로 PDK 활성 저해제는 치료하기 힘든 역분화 갑상선 암 치료제로 이용할 수 있고, 또한 역분화 갑상선 암에 대한 방사능 치료의 효능을 높일 수 있을 것으로 기대된다. Occurrence of the Warburg effect in solid tumors causes resistance to cancer chemotherapy, and targeting energy metabolisms such as aerobic glycolysis is a potential strategy for alternative treatment. Dichloroacetate (DCA), an inhibitor of pyruvate dehydrogenase kinase (PDK), shifts glucose metabolism from aerobic glycolysis to oxidative phosphorylation (OxPhos) in many cancers. In this study, we investigated the anticancer effect of DCA on a human anaplastic thyroid cancer (ATC) cell line, 8505C. We found that DCA selectively inhibits cell proliferation of the 8505C line but not of a normal thyroid line. In 8505C, the cell cycle was arrested at the G1/S phase with DCA treatment as a result of decreased antiapoptotic proteins such as HIF1α, PDK1, and Bcl-2 and increased proapoptotic proteins such as Bax and p21. DCA treatment enhanced the production of reactive oxygen species which consequently induced cell cycle arrest and apoptosis. Interestingly, DCA treatment not only reduced lactate production but also increased the expression of sodium-iodine symporter, indicating that it restores the OxPhos of glucose metabolism and the iodine metabolism of the ATC. Taken together, our findings suggest that PDK inhibitors such as DCA could be useful anticancer drugs for the treatment of ATC and may also be helpful in combination with chemotherapy and radiotherapy.
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베트남 자생식물 Engelhardia spicata Lechen ex Blume 추출물의 미백 효과
김욱철,박수빈,바흐 더 트란,응우 옌 투이,이승홍 한국응용생명화학회 2024 Journal of Applied Biological Chemistry (J. Appl. Vol.67 No.-
The aim of the current study was to investigate the whitening effect of extracts from 11 native plants in Vietnam for use as natural materials in cosmeceuticals. Firstly, tyrosinase inhibitory effect was evaluated to investigate the whitening effect of 11 plant extracts. As a result, Engelhardia spicata Lechen ex Blume extract (ESE) has shown the highest tyrosinase inhibitory effect. Therefore, ESE was used for subsequent experiments to clarify the whitening effect and its underlying mechanisms. ESE inhibited tyrosinase activity in a dose-dependent manner and the IC50 value of ESE against tyrosinase was 99 μg/mL. In addition, ESE significantly inhibited tyrosinase activity and reduced melanin contents dose-dependently in 3-isobutyl-1-methylaxanthine (IBMX)- stimulated B16F10 melanoma cells. ESE also downregulated the expression levels of key melanogenic proteins such as microphthalmia-associated transcription factor, tyrosinase-related protein 1, and tyrosinase in IBMX-stimulated B16F10 melanoma cells. In conclusion, these results firstly elucidate the antimelanogenesis effect of ESE in IBMX-induced melanoma cells. Taken together, our results demonstrate that ESE effectively inhibit melanogenesis, and could be applied in the fields of cosmeceuticals as a natural skin-whitening agent.
ScienceON
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