Licorice Ameliorates Cisplatin-Induced Hepatotoxicity Through Antiapoptosis, Antioxidative Stress, Anti-Inflammation, and Acceleration of Metabolism

Man, Qiong; Deng, Yi; Li, Pengjie; Ma, Jun; Yang, Zhijun; Yang, Xinggang; Zhou, Yan; Yan, Xiao Long

doi:10.3389/fphar.2020.563750

Cited by 32 publications

(19 citation statements)

References 61 publications

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“…For instance, crocin administration significantly decreased CP-mediated hepatotoxicity via down-regulating NF-κB and TGF-β signaling pathways (Khedr, Rahmo, Farag, Schaalan, & El Magdoub, 2020). It has been suggested that reducing apoptosis and oxidative stress can also effectively ameliorate CP-mediated hepatotoxicity (Man et al, 2020).…”

Section: Hepatotoxicitymentioning

confidence: 99%

Curcumin and its derivatives in cancer therapy: Potentiating antitumor activity of cisplatin and reducing side effects

Abadi

Mirzaei

Mahabady

et al. 2021

Phytotherapy Research

130

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Section: Hepatotoxicitymentioning

confidence: 99%

Curcumin and its derivatives in cancer therapy: Potentiating antitumor activity of cisplatin and reducing side effects

Abadi

Mirzaei

Mahabady

et al. 2021

Phytotherapy Research

130

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“…Likewise, Man et al. (2020) described the hepatotoxicity and promoted oxidative stress due to DDP, indicated by reduced SOD activity and increased MDA concentration. In contrast to overproduction of reactive radicals and plausible cell injury due to DDP treatment, berry polyphenols promote ROS‐mediated apoptosis of leukemia Jurkat cells (León‐González et al., 2015) while the combination of blueberry extracts and oxaliplatin promotes ROS production in colon cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Combination of cyanidin‐3‐O‐glucoside and cisplatin induces oxidative stress and apoptosis in HeLa cells by reducing activity of endogenous antioxidants, increasing bax/bcl‐2 mRNA expression ratio, and downregulating Nrf2 expression

Yang

et al. 2021

J Food Biochem

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Investigation on potentiation of existing drugs with natural compounds to enhance efficacy and reduce toxic effect of the drugs has been increasing in recent years. This paper reports cytotoxic effect (apoptosis‐related and oxidative stress‐related effect) of cyanidin‐3‐O‐glucoside (C3G), cisplatin (DDP), and their combination (C3G‐DDP) on cervical cancer HeLa cells. Concentration of intracellular reactive oxygen species (ROS) was determined by employing fluorescent marker 2′,7′‐dichlorodihydrofluorescein diacetate. On the other hand, malondialdehyde (MDA) and glutathione (GSH) concentration, and activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH‐Px) were quantitated by commercially available assay kits. C3G‐DDP significantly inhibited the activity of SOD, CAT, and GSH‐Px. Simultaneously, C3G‐DDP reduced GSH concentration while increased the concentration of ROS and MDA. Moreover, Western blot analysis suggested that C3G‐DDP significantly reduced the expression of nuclear factor erythroid 2‐related factor‐2 (Nrf2) and Nrf2 target proteins: heme oxygenase‐1 (HO‐1) and NAD(P)H quinone dehydrogenase 1 (NQO1). In contrast, C3G‐DDP increased the expression of Keap1. Furthermore, C3G‐DDP significantly upregulated and downregulated the mRNA expressions of bax and bcl‐2, respectively, thereby increasing bax/bcl‐2 mRNA expression ratio. Overall, our findings propose that potentiation of DDP with C3G improves cancer cell susceptibility, specifically cervical cancer cells, to DDP. Practical applications Cisplatin is recommended by most medical oncologists worldwide to treat cancer. Despite its neoplastic efficacy, it has undesirable side effects including nausea, vomiting, nephrotoxicity, and hepatotoxicity. Natural biologically active food ingredients are suggested to be used as antioxidants along with DDP therapy to prevent cisplatin‐induced toxicity. C3G‐DDP protected HeLa cells from oxidative stress by reducing NQO1 and HO‐1 levels and regulated the Nrf2 signaling pathway. In addition, C3G‐DDP protected HeLa cells from oxidative stress‐induced apoptosis by increasing bcl‐2 levels and decreasing bax levels. These results expanded our understanding of the role of C3G in a cervical cancer cell model, and provided a potential new treatment strategy for this cancer, as well as a theoretical basis for the development of new drugs in the future.

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“…One herb of Qingre Zaoshi Liangxue Fang (QRZSLXF) was Bletilla Striata and QRZSLXF could also treat UC by regulating the DOR- β -arrestin1-Bcl-2 signal transduction pathway [ 28 ]. Inflammation and oxidative stress in various diseases could be alleviated by the ingredients in YST, such as Scutellaria baicalensis [ 29 ] , Astragalus [ 30 ] , Atractylodes [ 31 ] , Licorice [ 32 ] , Penta-O-galloyl-β-d-glucose (obtained from Radix Paeoniae Alba) [ 33 ] , Cinnamon [ 34 ] , Mangiferin (obtained from Pueraria) [ 35 ] , Bletilla Striata [ 36 ] , and Casperome (extracted from Frankincense) [ 37 ]. In this study, we found that YST effectively suppressed TNBS-induced colonic inflammation showed by reversing changes in body weight, DAI, colonic length, and histological damage in the Model group.…”

Section: Discussionmentioning

confidence: 99%

Yu Shi An Chang Fang Ameliorates TNBS-Induced Colitis in Mice by Reducing Inflammatory Response and Protecting the Intestinal Mucosal Barrier

Lai

2021

Evidence-Based Complementary and Alternative Medicine

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Ulcerative colitis (UC) is an inflammatory bowel disease that is related to the occurrence of colon cancer. This study aimed to investigate the underlying mechanism by which Yu Shi An Chang Fang (YST) treated UC. 2, 4, 6-trinitrobenzene sulfonic acid (TNBS) was used to construct the UC model. The body weight, fecal viscosity, and fecal bleeding of all mice were recorded every day to calculate the DAI value. The pathological changes in colon tissues were observed by hematoxylin-eosin (H&E) staining. The levels of tumor necrosis factor-α (TNF-α), interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and myeloperoxidase (MPO) reflecting inflammation and the levels of malondialdehyde (MDA), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) reflecting oxidative stress in colon tissues were all measured by their assay kits. The mRNA expression of TNF-α, IL-1β, and IL-6 in colon tissues was detected by quantitative reverse transcription-PCR (qRT-PCR). The expression of proteins related to pyroptosis and the colonic mucosal barrier was analyzed by Western blot. As a result, TNBS caused decreases in body weight and colon lengths, triggered serious histological damage, promoted inflammation, oxidative stress, and pyroptosis, and destroyed the colonic mucosal barrier. The above changes caused by TNBS in colitis mice could be partially reversed by YST. In conclusion, YST ameliorates TNBS-induced UC in mice by reducing the inflammatory response and protecting the intestinal mucosal barrier.

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Licorice Ameliorates Cisplatin-Induced Hepatotoxicity Through Antiapoptosis, Antioxidative Stress, Anti-Inflammation, and Acceleration of Metabolism

Cited by 32 publications

References 61 publications

Curcumin and its derivatives in cancer therapy: Potentiating antitumor activity of cisplatin and reducing side effects

Curcumin and its derivatives in cancer therapy: Potentiating antitumor activity of cisplatin and reducing side effects

Combination of cyanidin‐3‐O‐glucoside and cisplatin induces oxidative stress and apoptosis in HeLa cells by reducing activity of endogenous antioxidants, increasing bax/bcl‐2 mRNA expression ratio, and downregulating Nrf2 expression

Yu Shi An Chang Fang Ameliorates TNBS-Induced Colitis in Mice by Reducing Inflammatory Response and Protecting the Intestinal Mucosal Barrier

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