Carcinogenesis promoting activity inside a xenograft tumor model. Results: In normal ovarian tissues, HSF1 was barely detected, whereas, higher expression of HSF1 was located in malignant EOC tissues. Suppressed proliferative activity and intensified apoptosis had been observed in HSF1 knocked-down SKOV3 cells. In nude mouse xenografts, downregulation of HSF1 was found to cause reduced carinogenesis, indicating the anti-tumor effect induced by modulation of HSF1 against EOC. Conclusions: Our findings suggest that HSF1 may perhaps be considered as a potential candidate to get a diagnostic marker of human EOC, and that modulation of HSF1 may very well be a promising therapy tactic against human EOC. Acknowledgements: Supported by National Natural Science Foundation of China (No. 81401216 and 81603189)Chin Med 2018, 13(Suppl 1):Page 29 ofReferences 1. Coward JI, Middleton K, Murphy F. Int J Womens Health. 2015;7: 89?03. two. Vihervaara A, Sistonen L. J Cell Sci. 2014;127:261?. 3. Chen Y, Chen J, Loo A, et al. Oncotarget. 2013;4:816?9.59 Protective effects of cyanidin3Oglucoside on carbon tetrachlorideinduced liver fibrosis along with the underlying mechanism in mice Triglycidyl isocyanurate In Vivo Xinwei Jiang1,two, Tianran Shen2, Xilan Tang2, Wenqi Yang2, Yan Yang2, Honghui Guo3, Wenhua Ling2,4 1 Division of Food Science and Engineering, Institute of Science and Technology, Jinan University, Guangzhou 510632, China; 2 Department of Nutrition, School of Public Health, Sun YatSen University, Guangzhou 510080, China; 3Department of Nutrition, Henry Fok School of Meals Science and Engineering, Shaoguan University, Shaoguan 512005, China; 4Guangdong Provincial Essential Laboratory of Food, Nutrition and Wellness, Guangzhou 510080, China Correspondence: Honghui Guo [email protected]; Wenhua Ling [email protected] Journal of Chinese Medicine 2018, 13(Suppl 1):59 Background: Preceding studies indicated that Cyanidin-3-O-glucoside (C3G) as a classical ACE Inhibitors products anthocyanin exerted liver protective impact, but the impact on liver fibrosis was not fully explored [1]. Additionally, the bioavailability of anthocyanins are fairly low, thus the mechanism of anti-fibrosis effect of C3G nonetheless have to be systematically investigated [2]. Components and strategies: Within the present study, carbon tetrachloride (CCl4)-treated liver fibrosis animal model and principal hepatic stellate cells (HSCs) have been adopted to discover the restraining effect of C3G and its metabolite protocatechuic acid (PCA) on liver fibrosis and also the activation of HSCs. Final results: Our information demonstrated that the remedy of C3G on CCl4-treated mice model inhibited liver fibrosis and HSCs activation. Both C3G and PCA reserved the lipid droplet at the same time as retinol in major HSCs in vitro. C3G and PCA separately inhibited the mRNA expression of -smooth muscle actin and collagen I, but elevated the amount of matrix metalloproteinase-2 and liver X receptors. Only PCA suppressed the levels of tumor necrosis aspect alpha (TNF-) and interleukin-6 (IL-6) secreted from HSCs substantially. Also, C3G and PCA inhibited the proliferation and migration of HSCs. Conclusions: In conclusion, daily intake of Cy-3-G could protect against liver fibrosis progression in mice induced by CCl4 via inhibiting HSC activation. PCA primarily explained the inhibiting effect, which offers a basis for clinical practice of liver fibrosis prevention. Funding: This function was funded by grants from the National Basic Research System (973 Program, 2012CB517506) and the National Nature Science Foundation (81372994). Ack.