Antitumor Effects of Astaxanthin on Esophageal Squamous Cell Carcinoma by up-Regulation of PPARγ

Cui, Lingling; Li, Zhonglei; Xu, Fan; Tian, Yalan; Chen, Tingting; Li, Jiaxin; Guo, Yingying; Lyu, Quanjun

doi:10.1080/01635581.2021.1952449

Cited by 7 publications

(6 citation statements)

References 38 publications

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“…AXT was discovered to increase radiosensitivity and trigger apoptosis in esophageal squamous epithelial cell carcinoma cells (LS-180 cells) by decreasing B-cell lymphoma 2 ( Bcl-2 ), CyclinB1 , cell division cycle 2 ( Cdc2 ) and favoring Bcl-2 associated X-protein ( Bax ) expression. By upregulating the expression of the genes Bax and Caspase-3 and downregulating the expression of the gene Bcl-2 , it has been discovered that AXT induces apoptosis in LS-180 cells and inhibits the growth and multiplication of cancer cells [ 58 ].…”

Section: Therapeutic Uses Of Axtmentioning

confidence: 99%

Production and therapeutic use of astaxanthin in the nanotechnology era

Abdelazim,

Ghit,

Assal

et al. 2023

Pharmacol. Rep

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Astaxanthin (AXT) is a red fat-soluble pigment found naturally in aquatic animals, plants, and various microorganisms and can be manufactured artificially using chemical catalysis. AXT is a xanthophyll carotenoid with a high potential for scavenging free radicals. Several studies have investigated AXT efficacy against diseases such as neurodegenerative, ocular, skin, and cardiovascular hypertension, diabetes, gastrointestinal and liver diseases, and immuno-protective functions. However, its poor solubility, low stability to light and oxygen, and limited bioavailability are major obstacles hindering its wide applications as a therapeutic agent or nutritional supplement. Incorporating AXT with nanocarriers holds great promise in enhancing its physiochemical properties. Nanocarriers are delivery systems with several benefits, including surface modification, bioactivity, and targeted medication delivery and release. Many approaches have been applied to enhance AXT’s medicinal effect, including solid lipid nanoparticles, nanostructured lipid carriers (NLCs) and polymeric nanospheres. AXT nano-formulations have demonstrated a high antioxidant and anti-inflammatory effect, significantly affecting cancer in different organs. This review summarizes the most recent data on AXT production, characterization, biological activity, and therapeutic usage, focusing on its uses in the nanotechnology era. Graphical abstract

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Section: Therapeutic Uses Of Axtmentioning

confidence: 99%

Production and therapeutic use of astaxanthin in the nanotechnology era

Abdelazim,

Ghit,

Assal

et al. 2023

Pharmacol. Rep

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show abstract

“…Besides, it is reported that in esophageal squamous cell carcinoma, AX has a protective effect on esophageal cancer by up-regulating PPAR-γ to activate the apoptotic pathway and inhibit oxidative stress [29]. However, the regulatory effect of AX on PPAR-γ in cerebral I/R injury is ill-defined.…”

Section: Discussionmentioning

confidence: 99%

Astaxanthin Regulates PPAR-<i>γ</i>/NF-<i>κ</i>B Pathway to Mitigate Nerve Injury after Cerebral Ischemia/Reperfusion in Rats

Huo¹,

Zhang²,

Zhao³

et al. 2022

JBM

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Purpose: This research evaluates the efficacy of astaxanthin (AX) on cerebral ischemia/reperfusion (I/R) injury in rats and elucidates the potential mechanism of its neuronal protective effect. Methods: Rats were subjected to a middle cerebral artery occlusion/reperfusion (MCAO/R) model. Fifty grown male Sprague-Dawley (SD) rats were divided into 5 groups, including sham operation group (Sham), MCAO/R group, MCAO/R+AX group, MCAO/R+ AX+ Scramble group and MCAO/R+AX+ si-PPAR-γ group. The neurological score and cerebral infarction volume were evaluated after surgery. Rat microglia (RM) were stimulated by lipopolysaccharide (LPS) to form an inflammatory environment. LPS-induced RM cells were incubated with different concentrations of AX (1, 5 or 10 µg/mL), then cell viability, the expression of microglial activation markers, including cytokines (IL-1β, IL-6 and TNF-α), cluster of differentiation 68 (CD68), inducible nitric oxide synthase (iNOS) and CD206 and the expression of PPAR-γ and phosphorylated P65 (p-P65) proteins were determined. Cells were treated with pcDNA-PPAR-γ, as well as treatment with si-PPAR-γ or PPAR-γ antagonist GW9662 before AX treatment, and then cell activation mediators were tested. Results: AX inhibits LPS-induced RM cells activation and enhanced the expression level of PPAR-γ protein in way of dose-dependent, and pcDNA-PPAR-γ treatment had the same effect as AX. While si-PPAR-γ transfection or PPAR-γ suppressant GW9662 treatment reversed the effect of AX, and cut down the level of PPAR-γ protein and augmented the level of p-P65 protein. In addition, AX treatment alleviated the infarct volume, and sensorimotor and cognitive functions of MCAO/R model rats. Conclusion: AX alleviates LPS-induced microglial injury and has a protective effect on rat cerebral I/R injury by regulating the PPAR-γ/NF-κB pathway.

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“…Numerous studies have shown that most tumor cells possess impaired antioxidant stress systems, and ROS significantly influence both cell death and survival[ 17 ]. Oxidative stress can lead to DNA base alterations, strand breaks, upregulation of proto-oncogenes, and downregulation of suppressor genes within cells, all of which are closely associated with the development of various tumors[ 12 ]. An imbalance between oxidants and antioxidants in the body is believed to critically contribute to this process (Figure 2 ).…”

Section: Features Of Esc Oxidative Stress In Escsmentioning

confidence: 99%

“…NPs have garnered considerable attention worldwide owing to their unique properties and potential medicinal value[ 11 ]. In recent decades, these compounds have become integral to drug discovery and development, playing crucial roles in cancer treatment[ 12 ]. Numerous active ingredients with anticancer activity have been discovered, and they act directly on tumor cells.…”

Section: Introductionmentioning

confidence: 99%

Targeting oxidative stress with natural products: A novel strategy for esophageal cancer therapy

Cao,

Zhang,

Guo

et al. 2024

World J Gastrointest Oncol

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Esophageal cancer (ESC) is a malignant tumor that originates from the mucosal epithelium of the esophagus and is part of the digestive tract. Although the exact pathogenesis of ESC has not been fully elucidated, excessive oxidative stress is an important characteristic that leads to the development of many cancers. Abnormal expression of several proteins and transcription factors contributes to oxidative stress in ESCs, which alters the growth and proliferation of ESCs and promotes their metastasis. Natural compounds, including alkaloids, terpenes, polyphenols, and xanthine compounds, can inhibit reactive oxygen species production in ESCs. These compounds reduce oxidative stress levels and subsequently inhibit the occurrence and progression of ESC through the regulation of targets and pathways such as the cytokine interleukins 6 and 10, superoxide dismutase, the NF-+ACY-kappa+ADs-B/MAPK pathway, and the mammalian Nrf2/ARE target pathway. Thus, targeting tumor oxidative stress has become a key focus in anti-ESC therapy. This review discusses the potential of Natural products (NPs) for treating ESCs and summarizes the application prospects of oxidative stress as a new target for ESC treatment. The findings of this review provide a reference for drug development targeting ESCs. Nonetheless, further high-quality studies will be necessary to determine the clinical efficacy of these various NPs.

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Antitumor Effects of Astaxanthin on Esophageal Squamous Cell Carcinoma by up-Regulation of PPARγ

Cited by 7 publications

References 38 publications

Production and therapeutic use of astaxanthin in the nanotechnology era

Production and therapeutic use of astaxanthin in the nanotechnology era

Astaxanthin Regulates PPAR-<i>γ</i>/NF-<i>κ</i>B Pathway to Mitigate Nerve Injury after Cerebral Ischemia/Reperfusion in Rats

Targeting oxidative stress with natural products: A novel strategy for esophageal cancer therapy

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Antitumor Effects of Astaxanthin on Esophageal Squamous Cell Carcinoma by up-Regulation of PPARγ

Cited by 7 publications

References 38 publications

Production and therapeutic use of astaxanthin in the nanotechnology era

Production and therapeutic use of astaxanthin in the nanotechnology era

Astaxanthin Regulates PPAR-&lt;i&gt;γ&lt;/i&gt;/NF-&lt;i&gt;κ&lt;/i&gt;B Pathway to Mitigate Nerve Injury after Cerebral Ischemia/Reperfusion in Rats

Targeting oxidative stress with natural products: A novel strategy for esophageal cancer therapy

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Astaxanthin Regulates PPAR-<i>γ</i>/NF-<i>κ</i>B Pathway to Mitigate Nerve Injury after Cerebral Ischemia/Reperfusion in Rats