The flavonoid hesperidin exerts anti-photoaging effect by downregulating matrix metalloproteinase (MMP)-9 expression via mitogen activated protein kinase (MAPK)-dependent signaling pathways

Lee, Hee Jeong; Im, A‐Rang; Kim, Su-Man; Kang, Hyung‐Sik; Lee, Jae Dong; Chae, Sungwook

doi:10.1186/s12906-017-2058-8

Cited by 63 publications

(51 citation statements)

References 38 publications

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“…Matrix metalloproteinase are important during healing of wounds and their higher expression after irradiation led to delay in the healing of wounds [61,86]. Hesperidin has been reported to reduce their expression that would have also augmented the healing of irradiated wounds in the present study [87].…”

Section: Histological Studiessupporting

confidence: 51%

Hesperidin, a Citrus Bioflavonoid Potentiates Repair and Regeneration of Deep Dermal Excision Wounds of Mice Whole Body Exposed to Different Doses of 60Co γ-Radiation

Gc¹

2018

CDOAJ

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Irradiation adversely affects the repair and regeneration of wounds causing negative impact on the clinical outcome. Therefore, it is necessary to screen newer paradigms that may help to mitigate the deleterious effects of ionizing radiations. Hesperidin (hesperitin-7-rhamnoglucoside or hesperitin-7-rutinoside), a predominant bioflavonoid found in citrus fruits has been evaluated for its wound healing activity in mice whole-body exposed to 2,4, 6 or 8 Gy of γ-radiation. A full-thickness skin wound was created on the dorsum of mice after exposure to various doses of γ-radiation and the wound repair and regeneration was assessed by capturing video images of the excision wounds periodically as a measure of wound contraction as well as by assessing the mean wound healing time. In addition, the biochemical profiles including collagen, hexosamine, DNA, and nitric oxide syntheses were estimated in the granulation tissues at various days postirradiation after exposure to 0 or 6 Gy. In a separate experiment histological information on fibroblast and blood vessel densities were collected in the regenerating granulation tissue at various post-irradiation days after 0 or 6 Gy irradiation. The whole-body exposure of mice to different doses of γ-radiation resulted in a dose dependent delay in the wound contraction and prolongation of wound healing time, where the highest delay was observed after 8 Gy irradiation. Administration of hesperidin orally before irradiation significantly reduced the radiation-induced delay in the wound contraction and mean wound healing time. The collagen, hexosamine, DNA and nitric oxide syntheses were significantly reduced after exposure to 6 Gy, whereas pretreatment with hesperidin significantly enhanced synthesis of collagen, hexosamine, DNA, and nitric oxide. Histological examination revealed an increased rise in fibroblast and vascular densities after treatment with hesperidin in comparison with 6 Gy irradiation. The study demonstrates that hesperidin treatment accelerated the healing of irradiated wounds by increasing the collagen, hexosamine, DNA, and nitric oxide syntheses and increasing the densities of fibroblasts and blood vessels in the

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Section: Histological Studiessupporting

confidence: 51%

Hesperidin, a Citrus Bioflavonoid Potentiates Repair and Regeneration of Deep Dermal Excision Wounds of Mice Whole Body Exposed to Different Doses of 60Co γ-Radiation

Gc¹

2018

CDOAJ

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“…Hesperidin has been shown to have anticancer effects promoting apoptosis in liver cancer [6] and bladder cancer [25]. Moreover, hesperidin inhibits the expression of MMP [10] and epithelial-mesenchymal transition (EMT) related proteins, suppressing cell migration and invasion [26], as well as being an anti-inflammatory [2]. In this study, we discovered that hesperidin decreases the expression of PD-L1 in cancer cells which contributes to tumor immune evasion.…”

Section: Discussionmentioning

confidence: 91%

“…It has already been reported that hesperidin induces anticancer activity through the promotion of apoptosis [9]. A recent report showed that hesperidin also inhibits epithelial-mesenchymal transition (EMT) and the expression of members of the MMP family, and thereby inhibiting cell invasion and contributing to its anticancer activity [10]. However, the role of hesperidin in inhibiting PD-L1 mediated immune checkpoint and ultimately increasing the tumor immune response, has yet to be investigated in breast cancer.…”

Section: Introductionmentioning

confidence: 99%

Inhibitory Effect of Hesperidin on the Expression of Programmed Death Ligand (PD-L1) in Breast Cancer

et al. 2020

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Programmed death ligand 1 (PD-L1) is overexpressed in the most aggressive breast cancer subtype, triple-negative breast cancer (TNBC), assisting the eradication of antitumor immunity, and thereby enhancing the survival of the tumor. This study explored how hesperidin affects PD-L1 expression, and thereby cancer progression in breast cancer cells. We found that MDA-MB231, the triple-negative breast adenocarcinoma cancer cell line, (high aggressiveness) has higher expression, in both mRNA and protein, of PD-L1 than that of the other breast cancer cell line, MCF-7 (low aggressiveness). Hesperidin inhibited cell proliferation in MDA-MB231 cells. Additionally, high expression of PD-L1 (both mRNA and protein) in aggressive cancer cells was strongly inhibited by hesperidin through inhibition of Akt and NF-κB signaling. Moreover, hesperidin treatment, by inhibiting activation of matrix metalloproteinases such as MMP-9 and MMP-2, suppressed the metastatic phenotype and cell migration in the PD-L1 high-expressing MDA-MB231 cells. In summary, hesperidin inhibits breast cancer cell growth through the inhibition of the expression of PD-L1 via downregulation of Akt and NF-κB signaling in TNBC. Moreover, hesperidin significantly suppresses cell migration of MDA-MB231 cells. Our findings reveal fresh insights into the anticancer effects of hesperidin which might have potential clinical implications.

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“…It can induce a variety of biological reactions, including cell proliferation, differentiation and apoptosis. Overexpression of various oncoproteins, such as chemokines and repressor proteins, was also reported to play a pivotal role in malignant transformation of cells (45,46). MAPK/ERK and MAPK/JNK have been currently found in mammals.…”

Section: Discussionmentioning

confidence: 99%

SIRT1 Expression and BRAF V600E Mutation in Papillary Thyroid Cancer: Implications for Diagnosis and Prognosis

Wang

et al. 2020

Preprint

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Background The BRAF V600E mutation is closely associated with aggressive clinicopathologic features and increased recurrence and disease-specific mortality of papillary thyroid cancer (PTC). Silent mating type information regulation 2 homolog-1 (SIRT1) has long been suggested to have tumor promotor activity and is strongly associated with the presence of BRAF mutations and higher grades of malignancy in many cancer types. However, no evidence or mechanism have been identified in PTC. Methods PTC tissue samples and their adjacent normal tissues from 42 PTC patients were collected; qRT-PCR, western blotting, T1799A BRAF mutation testing were utilized and the association with clinicopathologic features were assessed. Three different thyroid cell lines, Nthy-ori 3 − 1, TPC-1 and BCPAP, were used in in vitro studies. Cell counting kits and cell cycle analyses were utilized to investigate the level of cell proliferation and cell cycle progression. Transwell and Matrigel invasion assays were used to investigate the level of cell migration and invasion. Results SIRT1 is significantly upregulated in PTC, especially in lymph node metastatic and BRAF V600E-mutated patients. Cell counting kits and cell cycle analyses demonstrated that SIRT1 significantly promoted cell proliferation and cell cycle progression in BRAF V600E-mutated cells. Transwell and Matrigel invasion assays confirmed that SIRT1 promoted the migration and invasion ability of BRAF V600E-mutated cells. Additionally, the results of western blotting showed that the aberrant activation of the mitogen-activated protein kinase (MAPK) pathway played a crucial role in the tumor-promoting role of SIRT1 in BRAF V600E-mutated PTC biology. Conclusions SIRT1 expression with a BRAF V600E mutation may serve as new candidate targets for the diagnosis and treatment of papillary thyroid carcinomas.

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The flavonoid hesperidin exerts anti-photoaging effect by downregulating matrix metalloproteinase (MMP)-9 expression via mitogen activated protein kinase (MAPK)-dependent signaling pathways

Cited by 63 publications

References 38 publications

Hesperidin, a Citrus Bioflavonoid Potentiates Repair and Regeneration of Deep Dermal Excision Wounds of Mice Whole Body Exposed to Different Doses of 60Co γ-Radiation

Hesperidin, a Citrus Bioflavonoid Potentiates Repair and Regeneration of Deep Dermal Excision Wounds of Mice Whole Body Exposed to Different Doses of 60Co γ-Radiation

Inhibitory Effect of Hesperidin on the Expression of Programmed Death Ligand (PD-L1) in Breast Cancer

SIRT1 Expression and BRAF V600E Mutation in Papillary Thyroid Cancer: Implications for Diagnosis and Prognosis

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