Health-promoting effects of the citrus flavanone hesperidin

Li, Chaoyun; Schluesener, Hermann J.

doi:10.1080/10408398.2014.906382

Cited by 271 publications

(180 citation statements)

References 140 publications

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“…In this study, as shown in Figures 5 and 8, compared with model group, Nrf2 and its target genes (HO-1, NQO1, GST, and r-GCS) were up-regulated by TFCH treatments in vivo and in vitro, demonstrating the therapeutic mechanism of TFCH against NASH was related with Nrf-ARE signaling. Flavonoids product has numerous biological properties, which may be promising therapeutic agents for NASH (Li and Schluesener, 2017). Many natural products are rich in flavonoids and possess anti-oxidative and anti-inflammatory activities against NASH (Jian et al, 2018;Parafati et al, 2018;Wang et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Hepatoprotective and Anti-Oxidative Effects of Total Flavonoids From Qu Zhi Qiao (Fruit of Citrus Paradisi cv.Changshanhuyou) on Nonalcoholic Steatohepatitis In Vivo and In Vitro Through Nrf2-ARE Signaling Pathway

Shi

Liu

et al. 2020

Front. Pharmacol.

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Nonalcoholic steatohepatitis (NASH) is a liver disease defined as the dynamic condition of hepatocellular injury during the progress of nonalcoholic fatty liver disease (NAFLD). Total flavonoids from the dry and immature fruits of Citrus Paradisi cv.Changshanhuyou (accepted species name: Citrus × aurantium L) (Qu Zhi Qiao, QZQ) are purified and named TFCH. This study was purposed to investigate and analyze the effect of TFCH on NASH model through Nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response elements pathway in vivo and in vitro. In vivo study was performed using male C57BL/6 mice fed with high fat diet 16 weeks for NASH model. After 7-week modeling, mice in TFCH-treated group were daily treated with intragastric administration of TFCH at 25 mg/kg, 50 mg/kg, 200 mg/kg, respectively, for successive 8 weeks. Histopathological and immunohistochemical analyses were conducted for evaluating severity of NASH-mice model and the effect of TFCH treatment. In vitro experiment was performed by using human LX-2 cells and cultured with Free fatty acid (FFA) (Oleic acid: palmitic: l: 0.5 mmol/L) for 24 h and then treated with TFCH at different concentrations (0, 25, 50, 100, 200 mg/ml) for 6 h,12 h, and 24 h. Anti-apoptosis effect of TFCH on LX-2 cells cultured with FFA was revealed by the CCK-8 assay. Lipid parameters and oxidative stress markers were Frontiers in Pharmacology | www.frontiersin.org measured in vivo and in vitro, results showed that TFCH dose-dependently and greatly increased the antioxidant ability and reduced the oxidative damage in NASH model. The protein expression of Nrf2 and the downstream target genes in mice liver and human LX-2 cells were tested by Western blot analysis to investigate the possible molecular mechanisms of TFCH. Our results indicated that TFCH up-regulated protein expression of these genes and have the significant influence in activating the Nrf2-ARE signaling pathway. This study shows Nrf2-ARE signaling pathway may provide novel therapeutic opportunities for NASH therapy in the future.

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Section: Discussionmentioning

confidence: 99%

Hepatoprotective and Anti-Oxidative Effects of Total Flavonoids From Qu Zhi Qiao (Fruit of Citrus Paradisi cv.Changshanhuyou) on Nonalcoholic Steatohepatitis In Vivo and In Vitro Through Nrf2-ARE Signaling Pathway

Shi

Liu

et al. 2020

Front. Pharmacol.

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“…Phytochemicals, such as flavonoids of herbs and fruits showed chemopreventive effects against multiple human cancers . Hesperidin is a flavanone glycoside that is found in the Citrus species . It has been reported with antioxidant, anti‐inflammatory, and antifibrotic activities.…”

Section: Introductionmentioning

confidence: 99%

Involvement of PI3K/Akt pathway in the protective effect of hesperidin against a chemically induced liver cancer in rats

Mo’men

Hussein

Kandeil

2019

J Biochem & Molecular Tox

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Hesperidin is a flavanone glycoside that is found in the Citrus species and showed antioxidant, hepatoprotective as well as anticancer activity. This study investigated the effect of hesperidin on the PI3K/Akt pathway as a possible mechanism for its protective effect against diethylnitrosamine (DEN)‐induced hepatocellular carcinoma (HCC). Adult Wistar rats were divided into Control group (received drug vehicle); DEN group (received 100 mg/L of DEN solution for 8 weeks), and hesperidin + DEN group (received 200 mg/kg body weight of hesperidin/day orally for 16 weeks + DEN solution as DEN group). Our findings showed that the administration of hesperidin significantly decreased the elevation in liver function enzymes, serum AFP level, and oxidative stress markers. Moreover, hesperidin administration suppressed DEN‐induced upregulation of PI3K, Akt, CDK‐2 protein expression, and preserved the integrity of the liver tissues from HCC formation. In conclusion, the hepatoprotective activity of hesperidin is mediated via its antioxidation and downregulation of the PI3K/Akt pathway.

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“…The role of oxidative stress in UC has been documented as chronic intestinal inflammation is associated with reactive oxygen and nitrogen species leading to oxidative and nitrosative stress . Hesperetin‐7 rutinoside (HES) is one of the flavonoids that constitutes citrus fruits and is found naturally as glycosides . The microflora of the distal part of the small intestine and colon hydrolyses hesperidin into aglycones and hesperetin .…”

Section: Introductionmentioning

confidence: 99%

Hesperidin modulates dextran sulfate sodium‐induced ulcerative colitis in rats: Targeting sphingosine kinase‐1‐ sphingosine 1 phosphate signaling pathway, mitochondrial biogenesis, inflammation, and apoptosis

Shafik

Gaber

Mohamed

et al. 2019

J Biochem & Molecular Tox

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Ulcerative colitis (UC) is a chronic gastrointestinal disorder interfering with life quality. A total of 60 male Wistar rats were divided into four equal groups: Control (group I), hesperidin only (group II), UC untreated (group III), and UC treated with hesperidin (group IV). Hesperidin had modulatory effects on UC pathogenesis, which might be through alleviating colonic sphingosine phosphate phosphatase 2 messenger RNA expression and sphingosine kinase-1 levels, thus suppressing the subsequent downstream inflammatory and apoptotic cascades represented by decreased macrophage inflammatory protein-1α and enhancement of B-cell lymphoma 2 immunohistochemistry expression. Also, it improved mitochondrial biogenesis by increasing the peroxisome proliferator-activated receptor-gammacoactivator 1-α level. It successfully restored redox potential as evidenced by marked alleviations of the nitric oxide and peroxynitrite levels, increasing total antioxidant capacity, and activating the superoxide dismutase enzyme. Also, hesperidin alleviated the UC disease activity index and improved the histopathological picture. These findings may offer a new therapeutic strategy for UC treatment. K E Y W O R D S hesperidin, macrophage inflammatory protein-1 alpha, peroxisome proliferator-activated receptor-gamma-coactivator 1-α, sphingosine kinase, ulcerative colitis

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Health-promoting effects of the citrus flavanone hesperidin

Cited by 271 publications

References 140 publications

Hepatoprotective and Anti-Oxidative Effects of Total Flavonoids From Qu Zhi Qiao (Fruit of Citrus Paradisi cv.Changshanhuyou) on Nonalcoholic Steatohepatitis In Vivo and In Vitro Through Nrf2-ARE Signaling Pathway

Hepatoprotective and Anti-Oxidative Effects of Total Flavonoids From Qu Zhi Qiao (Fruit of Citrus Paradisi cv.Changshanhuyou) on Nonalcoholic Steatohepatitis In Vivo and In Vitro Through Nrf2-ARE Signaling Pathway

Involvement of PI3K/Akt pathway in the protective effect of hesperidin against a chemically induced liver cancer in rats

Hesperidin modulates dextran sulfate sodium‐induced ulcerative colitis in rats: Targeting sphingosine kinase‐1‐ sphingosine 1 phosphate signaling pathway, mitochondrial biogenesis, inflammation, and apoptosis

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