http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Nawong Boonnak,Suchada Chantrapromma,Supinya Tewtrakul,Teeratad Sudsai 대한약학회 2014 Archives of Pharmacal Research Vol.37 No.10
The inhibitory activity of extract and compoundsisolated from the roots of Cratoxylum formosumssp. pruniflorum against nitric oxide (NO) was evaluatedusing RAW264.7 cells. Isolation of the CH2Cl2 extract ofC. formosum ssp. pruniflorum roots afforded ten knownxanthones including six tri-oxygenated xanthones (1–6)and four tetra-oxygenated xanthones (7–10), respectively. Compound 7 showed the highest inhibitory activity againstNO release with an IC50 value of 3.9 lM, followed bycompound 8 with an IC50 value of 4.3 lM, respectively. Inorder to understand the mechanism of this anti-inflammatoryactivity, the transcriptional level of 7 was found todown regulate mRNA expressions of iNOS and COX-2 indose-dependent manners, whereas 8 inhibited only iNOSmRNA expression but did not affect on that of COX-2gene. Xanthones might be the main anti-inflammatorycomponents in C. formosum ssp. pruniflorum.
Kaewpiboon, Chutima,Boonnak, Nawong,Kaowinn, Sirichat,Chung, Young-Hwa Elsevier 2018 Bioorganic & medicinal chemistry letters Vol.28 No.4
<P><B>Abstract</B></P> <P>Multidrug resistance (MDR) cancer toward cancer chemotherapy is one of the obstacles in cancer therapy. Therefore, it is of interested to use formoxanthone C (1,3,5,6-tetraoxygenated xanthone; XanX), a natural compound, which showed cytotoxicity against MDR human A549 lung cancer (A549RT-eto). The treatment with XanX induced not only apoptosis- in A549RT-eto cells, but also autophagy-cell death. Inhibition of apoptosis did not block XanX-induced autophagy in A549RT-eto cells. Furthermore, suppression of autophagy by beclin-1 small interfering RNAs (siRNAs) did not interrupt XanX-induced apoptosis, indicating that XanX can separately induce apoptosis and autophagy. Of interest, XanX treatment reduced levels of histone deacetylase 4 (HDAC4) protein overexpressed in A549RT-etocells. The co-treatment with XanX and HDAC4 siRNA accelerated both autophagy and apoptosis more than that by XanX treatment alone, suggesting survival of HDAC4 in A549RT-eto cells. XanX reverses etoposide resistance in A549RT-eto cells by induction of both autophagy and apoptosis, and confers cytotoxicity through down-regulation of HDAC4.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Kaewpiboon Chutima,Boonnak Nawong,Kaowinn Sirichat,Yawut Natpaphan,Chung Young-Hwa 대한암예방학회 2022 Journal of cancer prevention Vol.27 No.2
Considering that presence of cancer stem cell (CSC) subpopulation in tumor tissues confers anticancer drug resistance, we investigated whether human A549 lung cancer cells resistant to etoposide possess CSC-like phenotypes. Furthermore, it is known that these malignant tumor features are the leading cause of treatment failure in cancer. We have thus attempted to explore new therapeutic agents from natural products targeting these malignancies. We found that formoxanthone C (XanX), a 1,3,5,6-tetraoxygenated xanthone from Cratoxylum formosum ssp. pruniflorum, at a non-cytotoxic concentration reduced the expression of the signal transducer and activator of transcription 1 (STAT1) and histone deacetylase 4 (HDAC4) proteins, leading to inhibition of CSC-like phenotypes such as cell migration, invasion, and sphere-forming ability. Moreover, we found that treatment with STAT1 or HDAC4 small interfering RNAs significantly hindered these CSC-like phenotypes, indicating that STAT1 and HDAC4 play a role in the malignant tumor features. Taken together, our findings suggest that XanX may be a potential new therapeutic agent targeting malignant lung tumors.