Journal Article10.1002/PTR.3503
Shikonin derivatives protect immune organs from damage and promote immune responses in vivo in tumour-bearing mice.
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TL;DR: Investigation of the antitumour and immunomodulatory effects of shikonin derivatives (ShD) in tumour‐bearing mice found it reduced the tumour load of tumour-bearing mice and protected the immune organs against tumours‐induced damage and immune function impairment.
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Abstract: Shikonin, a major component of Lithospermum erythrorhizon and Arnebia euchroma, exhibits antiinflammatory, immunomodulatory and antitumour activities. Although many recent studies have focused on the antitumour effects of shikonin, the exact mechanisms underlying its antitumour and immunomodulatory effects in tumour-bearing mice remain unclear. The aim of the present study was to investigate the antitumour and immunomodulatory effects of shikonin derivatives (ShD) in tumour-bearing mice. Swiss mice inoculated with hepatoma HepA22 or sarcoma 180 (S180) cells were treated with ShD or 5-fluorouracil (5Fu). Survival time, immune organs, natural killer cell activity, lymphocytes, lymphocyte transformation and interleukin (IL)-2 production were analysed. ShD significantly prolonged the survival (median survival time prolonged by >7 days) of tumour-bearing mice in a dose-dependent manner, inhibited the growth of transplantable neoplasms (inhibitory rate, > 33%), and recovered (at [ShD] = 2.5 mg/kg/day) or increased (at [ShD] > 5 mg/kg/day) the number of CD3- and CD19-positive cells. ShD also played a role in protecting the immune organs from damage and reversed or enhanced immune responses, as noted by the nearly normal thymic structure; enlarged splenic corpuscles; and improved natural killer cell activity, lymphocyte transformation and IL-2 production in ShD-treated mice. ShD reduced the tumour load of tumour-bearing mice and protected the immune organs against tumour-induced damage and immune function impairment. Copyright © 2011 John Wiley & Sons, Ltd.
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Citations
Immunogenic cell death and DAMPs in cancer therapy.
Dmitri V. Krysko,Abhishek D. Garg,Agnieszka Kaczmarek,Olga Krysko,Patrizia Agostinis,Peter Vandenabeele +5 more
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Shikonin derivatives for cancer prevention and therapy
TL;DR: Shikonin exerts additive and synergistic interactions in combination with established chemotherapeutics, immunotherapeutic approaches, radiotherapy and other treatment modalities, which further underscores the potential of this phytochemical to be integrated into standard treatment regimens.
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Shikonin-loaded antibody-armed nanoparticles for targeted therapy of ovarian cancer
Efthymia Iliana Matthaiou,Jaleh Barar,Raphael Sandaltzopoulos,Chunsheng Li,George Coukos,Yadollah Omidi +5 more
TL;DR: To limit its cytotoxic impact solely to tumor cells within the tumor microenvironment (TME), SHK was engineer as polymeric nanoparticles (NPs) with targeting moiety toward tumor microvasculature and proposed as a novel nanomedicine for targeted therapy of solid tumors.
Developing Phytocompounds from Medicinal Plants as Immunomodulators.
TL;DR: A selected group of medicinal herbs, their derived crude or fractionated phytoextracts and the specific phytochemicals/phytocompounds isolated from them, as well as categorized phytocompound groups with specific chemical structures are discussed in terms of their immunomodulatory bioactivities.
References
The tumor microenvironment and its role in promoting tumor growth.
TL;DR: The tumor microenvironment is created by the tumor and dominated by tumor-induced interactions, and various immune effector cells are recruited to the tumor site, their anti-tumor functions are downregulated, largely in response to tumor-derived signals.
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Induction of topoisomerase II-mediated DNA cleavage by the plant naphthoquinones plumbagin and shikonin.
TL;DR: Plumbagin and shikonin induced a similar DNA cleavage pattern with topoisomerase II which was different from the cleavage patterns induced with other known topoisomersase II-active drugs.
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Induction of apoptosis by shikonin through coordinative modulation of the Bcl-2 family, p27, and p53, release of cytochrome c, and sequential activation of caspases in human colorectal carcinoma cells.
TL;DR: It is suggested that shikonin-induced apoptosis is triggered by the release of cytochrome c into cytosol, procaspase-9 processing, activation of caspases-3, degradation of PARP, and DNA fragmentation caused by the casp enzyme-activated deoxyribonuclease through the digestion of DFF-45.
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Shikonin Induces Apoptosis through Reactive Oxygen Species/Extracellular Signal-Regulated Kinase Pathway in Osteosarcoma Cells
TL;DR: Results reveal that shikonin increased ROS generation and ERK activation, and reduced Bcl2, which consequently caused the cells to undergo apoptosis, which may be a promising chemotherapeutic agent for osteosarcoma treatment.
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Growth inhibition and induction of apoptosis in human oral squamous cell carcinoma Tca-8113 cell lines by shikonin was partly through the inactivation of NF-κB pathway
Ruan Min,Ji Tong,Yang Wenjun,Duan Wenhu,Zhou Xiaojian,He Jiacai,Zhou Jian,Chen Wan-tao,Zhang Chen-ping +8 more
TL;DR: Results raise the possibility that the anti‐tumor effects of Shikonin in Tca‐8113 cells are at least partly through the inactivation of the NF‐κB pathway and subsequent activation of protease caspase family.
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