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Ma F.,Tianjin Medical University | Hu L.,Tianjin Institute of Integrative Medicine for Acute Abdominal Diseases | Yu M.,Tianjin Medical University | Wang F.,Tianjin Institute of Integrative Medicine for Acute Abdominal Diseases
American Journal of Chinese Medicine | Year: 2016

Hypoxia-inducible factor-1 (HIF-1) is an (Formula presented.) dimeric transcription factor. Because HIF-1(Formula presented.) is instable with oxygen, HIF-1 is scarce in normal mammalian cells. However, HIF-1(Formula presented.) is expressed in pathological conditions such as cancer and obesity. Inhibiting HIF-1(Formula presented.) may be of therapeutic value for these pathologies. Here, we investigated whether emodin, derived from the herb of Rheum palmatum L, which is also known as Chinese rhubarb, and is native to China, regulates HIF-1(Formula presented.) expression. Male C57BL/6 mice without or with diet-induced obesity were treated with emodin for two weeks, while control mice were treated with vehicle. HIF-1(Formula presented.) expression was determined by Western blot. We found that emodin inhibited obesity-induced HIF-1(Formula presented.) expression in liver and skeletal muscle but did not regulate HIF-1(Formula presented.) expression in the kidneys or in intra-abdominal fat. In vitro, emodin inhibited HIF-1(Formula presented.) expression in human HepG2 hepatic cells and Y1 adrenocortical cells. Further, we investigated the mechanisms of HIF-1(Formula presented.) expression in emodin-treated HepG2 cells. First, we found that HIF-1(Formula presented.) had normal stability in the presence of emodin. Thus, emodin did not decrease HIF-1(Formula presented.) by stimulating its degradation. Importantly, emodin decreased the activity of the signaling pathways that led to HIF-1(Formula presented.) biosynthesis. Interestingly, emodin increased HIF-1(Formula presented.) mRNA in HepG2 cells. This may be a result of feedback in response to the emodin-induced decrease in the protein of HIF-1(Formula presented.). In conclusion, emodin decreases hepatic HIF-1(Formula presented.) by inhibiting its biosynthesis. © 2016 World Scientific Publishing Company

Yu M.,Tianjin Medical University | Liu H.,Tianjin Institute of Integrative Medicine for Acute Abdominal Diseases | Duan Y.,Tianjin Medical University | Duan Y.,Tianjin Institute of Integrative Medicine for Acute Abdominal Diseases | And 4 more authors.
Cancer Letters | Year: 2015

Increased fatty acids (FAs) regulate pancreatic cancer progression, however, the detailed mechanism is not clear, and different forms of FAs may play diversified roles in pancreatic cancer. To elucidate the underlying mechanism, we compared the effects of four major types of FAs on pancreatic cancer growth both in cell culture and in a mouse model. HPAF pancreatic cancer cells were implanted in nude mice for 14 weeks, and the mice were fed with four different high-fat/high-energy diets (15% fat, 4 kcal/g), an iso-caloric diet (5% fat, 4 kcal/g) and a normal diet (4% fat, 3 kcal/g). The high fat diets were rich in saturated fatty acids (SFAs), monounsaturated fatty acids (MUFAs), and n-6 and n-3 polyunsaturated fatty acids (n6- and n3PUFAs), respectively. While n3PUFA diet decreased tumor viability, the other high fat diets stimulated tumor viability by apparently different mechanisms. For instance, xenografts whose carriers were fed with SFA diet had marked expression of cancer-related proteins and lipid droplets. Although mice that were fed with MUFA- and n6PUFA diets had pancreatic tumors of similar size, liver metastasis occurred more frequently in those with the n6PUFA diet. In experiments in vitro, the HPAF-cell population was increased by SFAs and MUFAs, decreased by n3PUFAs and not changed by n6PUFAs. In conclusion, different fatty acids have different impact on pancreatic cancer cells. The effects of fatty acids on pancreatic cancer cells were consistent in vivo and in vitro except that n6PUFAs only had regulatory effects in vivo. © 2015 Elsevier Ireland Ltd.

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