Modified Lipid Nanocapsules for Targeted Tanshinone IIA Delivery in Liver Fibrosis

A network pharmacology approach to investigating the mechanism of Tanshinone IIA for the treatment of liver fibrosis

Journal of Ethnopharmacology ◽

10.1016/j.jep.2020.112689 ◽

2020 ◽

Vol 253 ◽

pp. 112689 ◽

Cited By ~ 2

Author(s):

Miao-Juan Shi ◽

Xiu-Li Yan ◽

Ben-Sheng Dong ◽

Wen-Na Yang ◽

Shi-Bing Su ◽

...

Keyword(s):

Liver Fibrosis ◽

Tanshinone Iia ◽

Network Pharmacology

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Enhanced oral bioavailability of Tanshinone IIA using lipid nanocapsules: Formulation, in-vitro appraisal and pharmacokinetics

International Journal of Pharmaceutics ◽

10.1016/j.ijpharm.2020.119598 ◽

2020 ◽

Vol 586 ◽

pp. 119598

Author(s):

Asmaa A. Ashour ◽

Alyaa A. Ramadan ◽

Doaa A. Abdelmonsif ◽

Amal H. El-Kamel

Keyword(s):

Oral Bioavailability ◽

Tanshinone Iia ◽

Lipid Nanocapsules

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Therapeutic Effect of Tanshinone IIA on Liver Fibrosis and the Possible Mechanism: A Preclinical Meta-Analysis

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2019/7514046 ◽

2019 ◽

Vol 2019 ◽

pp. 1-13

Author(s):

Qingji Ying ◽

Yangyang Teng ◽

Jing Zhang ◽

Zhenzhai Cai ◽

Zhanxiong Xue

Keyword(s):

Liver Fibrosis ◽

Liver Function ◽

Therapeutic Effect ◽

Animal Studies ◽

Meta Analysis ◽

Underlying Mechanism ◽

Tanshinone Iia ◽

Drug Preparation ◽

Clinical Drug

Background. Liver fibrosis is a serious human health problem, and there is a need for specific antifibrosis drugs in the clinic. Tanshinone IIA has recently been reported to have a role in the treatment of liver fibrosis. However, the evidence supporting its antifibrotic effect is not sufficient, and the underlying mechanism is not clear. We thus performed this meta-analysis of animal research to assess the therapeutic effect of tanshinone IIA on liver fibrosis and analyzed the possible associated mechanism to provide a reference for further clinical drug preparation and clinical research. Methods. We collect related articles from the databases PubMed, Web of Science, Embase, Wanfang, VIP, and CNKI. The quality of the included studies was evaluated according to the SYRCLE risk of bias tool for animal studies. Data were analyzed using RavMan 5.3 and Stata 12.0 software. Results. A total of 404 articles were retrieved from the databases. After screening, 11 articles were included in the analysis. The included studies’ methodological quality was generally low, and an obvious publication bias was found. The results showed that tanshinone IIA significantly improved liver function in experimental animals and reduced the level of liver fibrosis by reducing inflammation and inhibiting immunity, antiapoptotic processes, and HSC activation. Conclusion. Tanshinone IIA can effectively improve liver fibrosis and liver function in animal models and is worthy of future higher quality animal studies and clinical drug trials.

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Active Compounds Derived from Fuzheng Huayu Formula Protect Hepatic Parenchymal Cells from Apoptosis Based on Network Pharmacology and Transcriptomic Analysis

Molecules ◽

10.3390/molecules24020338 ◽

2019 ◽

Vol 24 (2) ◽

pp. 338 ◽

Cited By ~ 4

Author(s):

Rong Wu ◽

Shu Dong ◽

Fei-Fei Cai ◽

Xiao-Le Chen ◽

Meng-Die Yang ◽

...

Keyword(s):

Liver Fibrosis ◽

Cell Apoptosis ◽

Caspase 3 ◽

Stellate Cell ◽

Parenchymal Cell ◽

Transcriptomic Analysis ◽

Tanshinone Iia ◽

Network Pharmacology ◽

Active Compounds ◽

Parenchymal Cells

Fuzheng huayu formula (FZHY), an antifibrotic traditional Chinese medicine, is frequently used for the treatment of liver fibrosis. In this study, network analysis, transcriptomic analysis, assays of cell apoptosis, viability and protein expression were used for investigating the effects and mechanisms of compounds derived from FZHY on hepatic parenchymal cell (HPC) protection and hepatic stellate cell activation. Network pharmacology analysis found that 6 major compounds and 39 potential targets were important network nodes. Our analysis predicted that the active compounds of FZHY, including hederagenin, luteolin and tanshinone IIA inhibited cell apoptosis (p < 0.05), increased PI3K expression and reduced cleaved caspase 3 expression and the Bax/Bcl-w ratio (p < 0.05) in L02 cells that had apoptosis induced by TNF-α. Few significant changes caused by FZHY, hederagenin, luteolin and tanshinone IIA were observed in hepatic stellate Lx2 cells upon TGF-β1 induction. These data suggest that FZHY is active against liver fibrosis, protects hepatic parenchymal cells from apoptosis, and recovers liver function, possibly through the effects of its active compounds hederagenin, luteolin and tanshinone IIA and is involved in the inhibition of apoptosis in HPCs, possibly through regulating the PI3K, ERK, cleaved caspase 3 and Bax/Bcl-w levels.

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Tanshinone IIA attenuates elastase-induced AAA in rats via inhibition of MyD88-dependent TLR-4 signaling

VASA ◽

10.1024/0301-1526/a000326 ◽

2014 ◽

Vol 43 (1) ◽

pp. 39-46 ◽

Cited By ~ 16

Author(s):

Tao Shang ◽

Feng Ran ◽

Qian Qiao ◽

Zhao Liu ◽

Chang-Jian Liu

Keyword(s):

Nuclear Factor Κb ◽

Tanshinone Iia ◽

Myeloid Differentiation ◽

Aortic Tissue ◽

Toll Like Receptor ◽

Sprague Dawley ◽

Toll Like Receptor 4 ◽

Tissue Samples ◽

Myeloid Differentiation Factor ◽

And Control

Background: The purpose of this study was to determine whether myeloid differentiation factor88-dependent Toll-Like Receptor-4 (TLR-4) signaling contributed to the inhibition of abdominal aortic aneurysm (AAA) by Tanshinone IIA (Tan IIA). Materials and methods: Male Sprague-Dawley rats (n = 12 / group) were randomly distributed into three groups: Tan IIA, control, and sham. The rats from Tan IIA and control groups under-went intra-aortic elastase perfusion to induce AAAs, and those in the sham group were perfused with saline. Only the Tan IIA group received Tan IIA (2 mg / rat / d). Aortic tissue samples were harvested at 24 d after perfusion and evaluated using reverse transcriptase-polymerase chain reaction, Western blot, immunohistochemistry and immunofluorescence. Results: The over-expression of Toll-Like Receptor-4 (TLR-4), Myeloid Differentiation factor 88 (MyD88), Phosphorylated Nuclear Factor κB (pNF-κB) and Phosphorylated IκBα (pIκBα) induced by elastase perfusion were significantly decreased by Tan IIA treatment. Conclusions: Tan IIA attenuates elastase-induced AAA in rats possibly via the inhibition of MyD88-dependent TLR-4 signaling, which may be one potential explanation of why Tan IIA inhibits AAA development through multiple effects.

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