PMID- 30497486 OWN - NLM STAT- MEDLINE DCOM- 20190201 LR - 20190201 IS - 1476-511X (Electronic) IS - 1476-511X (Linking) VI - 17 IP - 1 DP - 2018 Nov 30 TI - Fufang-Zhenzhu-Tiaozhi Capsule reduces restenosis via the downregulation of NF-kappaB and inflammatory factors in rabbits. PG - 272 LID - 10.1186/s12944-018-0921-3 [doi] LID - 272 AB - BACKGROUND: To investigate the effects of a Chinese herbal medicine Fufang-Zhenzhu Tiaozhi Capsule (FTZ) on restenosis and elucidate the mechanism of action. METHODS: A restenosis model was established by balloon rubbing the endothelium of the abdominal aorta followed by high fat diet. Rabbits were divided into blank control group, restenosis group, FTZ group (0.66 mg/kg/day), atorvastatin group (5 mg/kg/day) and FTZ + atorvastatin group (n = 8). Vascular stenosis was analyzed by X-ray. Serum levels of chemokines and cytokines interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-12 (IL-12), C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-alpha), monocyte chemoattractant protein-1 (MCP-1), and intercellular adhesion molecule-1 (ICAM-1) were measured by ELISA. The levels of NF-kappaB, IkappaB-alpha, P-IkappaBalpha, IKK-alpha, and P-IKKalpha/beta from injured abdominal arteries were detected by Western blotting. RESULTS: Restenosis was induced successfully via abdominal artery balloon injuries and high fat diet. Restenosis was significantly decreased in FTZ group compared with restenosis group (P < 0.05). FTZ group had markedly reduced serum lipid levels (P < 0.05). In addition, the levels of TNF-alpha, IL-1, IL-6, IL-8, IL-12, ICAM-1 and MCP-1 decreased by FTZ treatment (P < 0.05). The expression of NF-kappaB in the atherosclerotic lesions was significantly attenuated in FTZ group (P < 0.05). CONCLUSION: FTZ could reduce restenosis via reducing NF-kappaB activity and inflammatory factor expression within the atherosclerotic lesion in a rabbit restenosis model. FTZ may be a new therapeutic agent for restenosis. FAU - Zhang, Rendan AU - Zhang R AD - Department of Cardiology, Boai Hospital of Zhongshan, Zhongshan, 528403, China. FAU - Li, Tudi AU - Li T AD - Department of Cardiology, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, 510080, Guangdong, China. FAU - Guo, Jiao AU - Guo J AD - Department of Cardiology, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, 510080, Guangdong, China. FAU - Zhao, Yanqun AU - Zhao Y AD - Department of Cardiology, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, 510080, Guangdong, China. FAU - Liu, Yuhong AU - Liu Y AD - Department of Cardiology, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, 510080, Guangdong, China. FAU - Yao, Yusi AU - Yao Y AD - Department of Cardiology, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, 510080, Guangdong, China. FAU - Zeng, Zhihuan AU - Zeng Z AD - Department of Cardiology, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, 510080, Guangdong, China. gzzh@163.com. LA - eng PT - Journal Article DEP - 20181130 PL - England TA - Lipids Health Dis JT - Lipids in health and disease JID - 101147696 RN - 0 (Chemokine CCL2) RN - 0 (Drugs, Chinese Herbal) RN - 0 (Interleukin-1) RN - 0 (Interleukin-6) RN - 0 (Interleukin-8) RN - 0 (NF-kappa B) RN - 0 (Tumor Necrosis Factor-alpha) RN - 187348-17-0 (Interleukin-12) RN - 9007-41-4 (C-Reactive Protein) RN - A0JWA85V8F (Atorvastatin) SB - IM MH - Animals MH - Aorta, Abdominal/drug effects MH - Atherosclerosis/*drug therapy/genetics/physiopathology MH - Atorvastatin MH - C-Reactive Protein/genetics MH - Chemokine CCL2/genetics MH - Coronary Restenosis/*drug therapy/genetics/physiopathology MH - Diet, High-Fat/adverse effects MH - Disease Models, Animal MH - Drugs, Chinese Herbal/*administration & dosage MH - Endothelium/drug effects/physiopathology MH - Gene Expression Regulation/drug effects MH - Humans MH - Inflammation/*drug therapy/genetics/physiopathology MH - Interleukin-1/genetics MH - Interleukin-12/genetics MH - Interleukin-6/genetics MH - Interleukin-8/genetics MH - NF-kappa B/genetics MH - Rabbits MH - Tumor Necrosis Factor-alpha/genetics PMC - PMC6267089 OTO - NOTNLM OT - Animal model OT - FTZ OT - Inflammation OT - NF-kappaB OT - Restenosis COIS- ETHICS APPROVAL: All animal procedures were performed in accordance with the protocols approved by the Committee for Supervision of Animal Experiments of Guangdong Pharmaceutical University (Guangzhou, China). CONSENT FOR PUBLICATION: Not applicable. COMPETING INTERESTS: The authors declare that they have no competing interests. PUBLISHER'S NOTE: Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. EDAT- 2018/12/01 06:00 MHDA- 2019/02/02 06:00 PMCR- 2018/11/30 CRDT- 2018/12/01 06:00 PHST- 2018/09/21 00:00 [received] PHST- 2018/11/20 00:00 [accepted] PHST- 2018/12/01 06:00 [entrez] PHST- 2018/12/01 06:00 [pubmed] PHST- 2019/02/02 06:00 [medline] PHST- 2018/11/30 00:00 [pmc-release] AID - 10.1186/s12944-018-0921-3 [pii] AID - 921 [pii] AID - 10.1186/s12944-018-0921-3 [doi] PST - epublish SO - Lipids Health Dis. 2018 Nov 30;17(1):272. doi: 10.1186/s12944-018-0921-3.