Isolates from <scp>Alpinia officinarum</scp> Hance attenuate LPS‐induced inflammation in HepG2: Evidence from in silico and in vitro studies

Elgazar, Abdullah A.; Selim, Nabil Mohamed; Abdel-Hamid, Nabil Mohie; El-Magd, Mohammed A.; El-Hefnawy, Hala M

doi:10.1002/ptr.6056

Cited by 57 publications

(35 citation statements)

References 46 publications

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“…Another possible way by which cancer cells maintain their high proliferative capacity and survival, is induction of inflammation [37]. Therefore, inhibition of inflammation is an urgent need for killing cancer cells.…”

Section: Samples Collection and Preparationmentioning

confidence: 99%

The potential therapeutic effect for melatonin and mesenchymal stem cells on hepatocellular carcinoma

et al. 2019

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Background/aim: Herein, we investigated the potential therapeutic effect of Melatonin (Mel) and/or mesenchymal stem cells (MSCs) on rat model of HCC. Materials and Methods: Female mature rats were divided into 5 groups (n = 10/group): normal (Nor), HCC group intraperitoneally injected with 200 mg/kg DEN, and 3 treated groups; HCC + Mel (Mel) group given Mel intraperitoneally 20 mg/kg, twice a week, HCC + MSCs (MSCs) group intravenously injected by 1 × 106 cells, and HCC + MSCs (Mel +MSCs) group. Results: Rats in HCC group showed most deteriorated effect in form of increased mortality and relative liver weight, elevated serum levels of ALT, AST, ALP, AFP and GGT in addition to increased pre-neoplastic nodules in liver tissues. Liver tissues of HCC group also exhibited lower level of apoptosis as indicated by decreased DNA fragmentation and expression of p53 caspase 9 and caspase 3 genes and increased PCNA immunoreactivity. Moreover, in this group the expression of IL6 and TGFβ1 genes was significantly upregulated. All these deleterious effects induced by DEN were reversed after administration of Mel and/ or MSCs with best improvement for the combined group (MSCs + Mel). Conclusions: These findings reveal a better therapeutic effect for MSCs when given with Mel and we attribute this beneficial effect, at least in part, to triggering apoptosis and targeting inflammation in HCC. Therefore, combined treatment with Mel and MSCs is recommended to enhance the therapeutic potential against HCC.

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Section: Samples Collection and Preparationmentioning

confidence: 99%

The potential therapeutic effect for melatonin and mesenchymal stem cells on hepatocellular carcinoma

et al. 2019

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“…These compounds down-regulated the gene expression of IL-6, IL-1β, pro-inflammatory cytokines and TNF-α in a dose-dependent manner. This indicates that these isolated compounds may be a promising treatment for other inflammatory diseases [75].…”

Section: Alpinia Officinarummentioning

confidence: 85%

Herbal management of hepatocellular carcinoma through cutting the pathways of the common risk factors

Abdel-Hamid

Abass

Mohamed

et al. 2018

Biomedicine & Pharmacotherapy

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Hepatocellular carcinoma (HCC) is considered the most frequent tumor that associated with high mortality rate. Several risk factors contribute to the pathogenesis of HCC, such as chronic persistent infection with hepatitis C virus or hepatitis B virus, chronic untreated inflammation of liver with different etiology, oxidative stress and fatty liver disease. Several treatment protocols are used in the treatment of HCC but they also associated with diverse side effects. Many natural products are helpful in the co-treatment and prevention of HCC. Several mechanisms are involved in the action of these herbal products and their bioactive compounds in the prevention and co-treatment of HCC. They can inhibit the liver cancer development and progression in several ways as protecting against liver carcinogens, enhancing effects of chemotherapeutic drugs, inhibiting tumor cell growth and metastasis, and suppression of oxidative stress and chronic inflammation. In this review, we will discuss the utility of diverse natural products in the prevention and co-treatment of HCC, through its capturing of the common risk factors known to lead to HCC and shed the light on their possible mechanisms of action. Our theory assumes that shutting down the risk factor to cancer development pathways is a critical strategy in cancer prevention and management. We recommend the use of these plants side by side to recent chemical medications and after stopping these chemicals, as a maintenance therapy to avoid HCC progression and decrease its global incidence.

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“…These inflammatory cytokines lead to the activation of signaling pathways that ultimately impair insulin signaling (Hirabara et al, ; Luca & Olefsky, ). Moreover, some factors involved in inflammatory processes also can impair insulin sensitivity, such as lipopolysaccharide (LPS; Elgazar, Selim, Abdel‐Hamid, El‐Magd, & El Hefnawy, ; Jung, Chung, Kim, Abd, & Jeong, ; Saad, Santos, & Prada, ).…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, some factors involved in inflammatory processes also can impair insulin sensitivity, such as lipopolysaccharide (LPS; Elgazar, Selim, Abdel-Hamid, El-Magd, & El Hefnawy, 2018;Jung, Chung, Kim, Abd, & Jeong, 2018;Saad, Santos, & Prada, 2016).…”

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confidence: 99%

Hesperidin ameliorates insulin resistance by regulating the IRS1‐GLUT2 pathway via TLR4 in HepG2 cells

Tian

Liu

et al. 2019

Phytotherapy Research

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The aim of this study was to evaluate the effect and mechanism of hesperidin (HES) on insulin resistance (IR) in the human hepatocellular carcinoma cell line (HepG2 cells). HepG2 cells were induced with lipopolysaccharide (LPS) as a model of IR and treated with HES at three dosages. Next, the levels of interleukin‐6 (IL‐6) and tumor necrosis factor‐α (TNF‐α), the glucose content, and glucose uptake were evaluated by enzyme‐linked immunosorbent assay, glucose oxidase‐peroxidase method (GOD‐POD), or (2‐(N‐(7‐nitrobenz‐2‐oxa‐1, 3‐diazol‐4‐yl)amino)‐2‐deoxyglucose) (2‐NBDG). Moreover, the protein expression of toll‐like receptors 4 (TLR4), insulin receptor substrate 1 (IRS1), nuclear factor kappa B (NF‐κB), and glucose transporter 2 (GLUT2) in HepG2 cells treated with HES were assessed via western blotting analysis. In addition, GLUT2 protein expression exposed to HES was detected following treatment with TLR4 inhibitor (HTA125). Our results demonstrated that HES decreased the levels of TNF‐α and IL‐6, attenuated the glucose content in culture medium and increased glucose uptake in insulin‐resistant HepG2 cells in vitro. Moreover, HES upregulated the expression of IRS1 and GLUT2 protein and downregulated the protein expression of TLR4 and NF‐κB in insulin‐resistant HepG2 cells. The expression of GLUT2 protein had no significant changes when treated with HES after blockade of TLR4. HES attenuated IR in LPS‐inducedinsulin‐resistant HepG2 cells. Therefore, regulating the IRS1‐GLUT2 pathway via TLR4 represents a potential mechanism of HES on IR in HepG2 cells.

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Isolates from Alpinia officinarum Hance attenuate LPS‐induced inflammation in HepG2: Evidence from in silico and in vitro studies

Cited by 57 publications

References 46 publications

The potential therapeutic effect for melatonin and mesenchymal stem cells on hepatocellular carcinoma

The potential therapeutic effect for melatonin and mesenchymal stem cells on hepatocellular carcinoma

Herbal management of hepatocellular carcinoma through cutting the pathways of the common risk factors

Hesperidin ameliorates insulin resistance by regulating the IRS1‐GLUT2 pathway via TLR4 in HepG2 cells

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