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04 포스터 발표 : 농식품 환경분야(PF) ; PF-02 : 찔레꽃 메탄올 추출물의 프리라디칼소거 활성
강선철 ( Sun Chul Kang ),모니카 ( Monika Bhardwaj ),바후구나 ( Ashutosh Bahuguna ) 한국환경농학회 2015 한국환경농학회 학술대회집 Vol.2015 No.-
Living beings possess an innate antioxidant enzymes defense mechanism to protect the biological molecules from detrimental effects of these reactive oxygen species (ROS). However, during intense oxidative stress, where the pro-oxidants, antioxidant defence system become insufficient to control it, as a reason persist high level of oxidative stress remains, which is responsible for the pathological conditions such as cancer, aging, rheumatoid arthritis, atherosclerosis and neurodegenerative diseases. To balance such an oxidative stress condition an external antioxidant source are required. In view of the above, present study was carried out to investigate the in vitro antioxidant potential of the metahanolic extract of Rosa multiflora flowers. The in vitro antioxidant activity of the different concentration of R.multiflora methanol extract (RMA) was determined by the DPPH● and ABTS●+ radical scavenging method. A significant DPPH● radical scavenging activity was observed in different concentration of RMA as compare to control with the IC50 value of 15.2±0.7 μg/ml. Further more, the antioxidant capacity of RMAwas evaluated by ABTS●+ radical scavenging activity at different concentrations. Finding suggests a significant scavenging activity toward ABTS●+ radicals in a concentration dependent manner, with the IC50 value of 7.42±0.63 μg/ml.
Khaket, Tejinder Pal,Singh, Mahendra Pal,Khan, Imran,Bhardwaj, Monika,Kang, Sun Chul Elsevier 2018 Cellular signalling Vol.46 No.-
<P><B>Abstract</B></P> <P>As Autophagy is a pivotal mechanism of cancer cell survival and the development of chemotherapeutic resistance; therefore, new approaches are warranted for its targeting which may be fulfilled by cathepsins regulation. Amongst cathepsins, cathepsin C (CTSC) is highly expressed in various cancers and possesses significant therapeutic potential in autoimmune disorders; however, its role in colorectal cancer has not been explored. Herein, we aimed to investigate the role of CTSC in autophagy regulation mediated colorectal carcinoma cell proliferation. Cathepsin C targeting through inhibitors/siRNA leads to the accumulation of light chain 3 II and p62 without affecting the lysosomal integrity, revealed dysfunctional autolysosomal degradation which is also substantiated by proteolytic studies. Cathepsin C inhibition showed comparable autophagy blockade with E64d and augmented the autophagy blockade mediated by bafilomycin. Loss of CTSC function also induced ER stress-mediated JNK phosphorylation accompanied by the translocation of mitochondrial cyt <I>c</I> followed by apoptotic cell death in colorectal carcinoma cells. Taken together, the study reveals that CTSC targeting plays a key role in the regulation of autophagy mediated colorectal cancer cell proliferation. Further investigations are required to determine the functional role of CTSC in other tumors also which may have implications for the therapeutic prevention of cancer in the future.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Cathepsin C targeting leads to the accumulation of autophagolysosomes which supported the key role of cathepsin C activity in autophagy regulation. </LI> <LI> Cathepsin C inhibition augmented the autophagy blockade caused by bafilomycin. </LI> <LI> In colorectal cancer cells, cathepsin C inhibition induced ER-stress and JNK signaling mediated apoptosis in HCT-116 cells. </LI> <LI> GFDMK treated cells enhances the sensitivity of colorectal cells toward E64d. </LI> </UL> </P>