Cannabinoid receptors are involved in the protective effect of a novel curcumin derivative C66 against CCl4-induced liver fibrosis
| Autor: | Xiao-Dong Wang, Yong-Ping Chen, Zhen-Ping Yu, Shan-Jie Du, Da-zhi Chen, Rui-Cong Chen, Jia-Jia Dong, He Wu, Si-Si Huang, Lanman Xu, Wenke Feng, Guang Liang, Yong-Ping Yang |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
Liver Cirrhosis
Male 0301 basic medicine Curcumin Cannabinoid receptor Pharmacology Mice 03 medical and health sciences chemistry.chemical_compound Fibrosis Hepatic Stellate Cells Cannabinoid receptor type 2 medicine Animals Receptors Cannabinoid Receptor Carbon Tetrachloride Chemistry JNK Mitogen-Activated Protein Kinases NF-kappa B NF-κB medicine.disease Mice Inbred C57BL Protein Transport 030104 developmental biology Gene Expression Regulation Liver Cytoprotection Hepatic stellate cell Signal transduction Signal Transduction |
| Zdroj: | European Journal of Pharmacology. 779:22-30 |
| ISSN: | 0014-2999 |
| Popis: | Liver fibrosis is one of the major causes of morbidity and mortality worldwide and lacks efficient therapy. Recent studies suggest the curcumin protects liver from fibrosis. However, curcumin itself is in low bioavailable concentration when administered orally, and the protective mechanism remains poorly understood. The current study aimed to investigate whether a more stable derivative of curcumin, C66, protects against CCl4-inudced liver fibrosis and examine the underlying mechanism involving cannabinoid receptor (CB receptor). At a dose lower than curcumin itself, C66 displayed a superior anti-fibrotic effect. C66 significantly reduced collagen deposition, pro-inflammatory cytokine expression, and liver enzyme activities. Mechanistic study revealed that C66 treatment decreased CCl4-induced cannabinoid receptor 1 (CB1 receptor) expression and increased cannabinoid receptor 2 (CB2 receptor) expression, along with an inhibition of JNK/NF-κB-mediated inflammatory signaling. In conclusion, this curcumin derivative attenuates liver fibrosis likely involving a CB/JNK/NF-κB-mediated pathway. |
| Databáze: | OpenAIRE |
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