Squid Ink Polysaccharides Protect Human Fibroblast Against Oxidative Stress by Regulating NADPH Oxidase and Connexin43

Chen, Ying; Liu, Huazhong; Huang, Hao; Ma, Yu-Bin; Wang, Ruihua; Hu, Yong; Zheng, Xiufen; Chen, Chunmei; Tang, Hongfeng

doi:10.3389/fphar.2019.01574

Cited by 19 publications

(7 citation statements)

References 50 publications

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“…In contrast, SOD, along with GSH-Px, is an effective ROS scavenger. Increased levels of ROS re ect the ability to resist oxidative damage [41]. In the induced POI model, the expression of oxidative stress products (ROS, T-AOC, and MDA) increased, whereas that of antioxidant products (SOD and GSH-Px) decreased.…”

Section: Discussionmentioning

confidence: 99%

Quercetin alleviates cyclophosphamide-induced premature ovarian insufficiency in mice by reducing mitochondrial oxidative stress and pyroptosis in granulosa cells

Chen

Zhao

Miao

et al. 2022

Preprint

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Background: Exposure to cyclophosphamide (CTX) induces premature ovarian insufficiency (POI). Quercetin is a natural flavonoid that exhibits anti-inflammatory and antioxidant properties, and its antioxidant activity is correlated with POI. However, the mechanism underlying its protective role in CTX-induced ovarian dysfunction is unclear. This study aimed to explore whether quercetin can protect ovarian reserves by activating mitochondrial biogenesis and inhibiting pyroptosis. Methods: Thirty-six female C57BL/6 mice were randomly subdivided into six groups. Except for the control group, all groups were injected with 90 mg/kg CTX to establish a POI model and further treated with coenzyme 10 or various doses of quercetin. The mice were sacrificed 48 h after 10 IU pregnant mare serum gonadotropin was injected four weeks after treatments. We used enzyme-linked immunosorbent assays to detect serum hormone expression and light and transmission electron microscopy to assess ovarian tissue morphology and mitochondria. Additionally, we tested oxidant and antioxidant levels in ovarian tissues and mitochondrial function in granulosa cells (GCs). The expression of mitochondrial biogenesis and pyroptosis-related proteins and mRNA was analyzed using western blotting and RT-qPCR. Results: Quercetin elevated serum anti-Müllerian hormone, estradiol, and progesterone levels, decreased serum follicle-stimulating hormone and luteinizing hormone levels, and alleviated ovarian pathology. It reduced the mitochondrial DNA content and mitochondrial membrane potential. Furthermore, it upregulated ATP levels and the mRNA and protein expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α), mitochondrial transcription factor A, and superoxide dismutase 2. In addition, it suppressed NOD-like receptor pyrin domain containing 3, caspase-1, interleukin-1β, and gasdermin D levels in the GCs of POI mice. Conclusions: Quercetin protected the ovarian reserve from CTX-induced ovarian damage by reversing mitochondrial dysfunction and activating mitochondrial biogenesis via the PGC1-α pathway. Moreover, quercetin may improve ovarian functions by downregulating pyroptosis in the CTX-induced POI model. Thus, quercetin can be considered a potential agent for treating POI.

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Section: Discussionmentioning

confidence: 99%

Quercetin alleviates cyclophosphamide-induced premature ovarian insufficiency in mice by reducing mitochondrial oxidative stress and pyroptosis in granulosa cells

Chen

Zhao

Miao

et al. 2022

Preprint

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“…Furthermore, Gu et al [34]found that SIP has the capability to reduce levels of reactive oxygen species (ROS) and malondialdehyde (MDA) content in the testes of male mice, enhance superoxide dismutase (SOD) activity, and protect the normal functioning of mitochondria.. Our team's extracted polysaccharides were found to have similar composition and functionality to those extracted by other researchers. It was also demonstrated that SIP exhibits a strong antioxidant effect and the ability to inhibit H 2 O 2 -induced oxidative stress in normal human skin broblasts [12], which prompted us to explore more deeply whether SIP could play a role in cellular in ammation and realize new applications of SIP in in ammatory dermatoses.…”

Section: Discussionmentioning

confidence: 99%

Squid Ink Polysaccharides inhibit TSLP expression via the Piezo 1-Ca2+-NFAT1 signaling to ameliorate Atopic Dermatitis

Wen,

Liu,

Deng

et al. 2024

Preprint

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Atopic dermatitis (AD) is a chronic and recurrent inflammatory dermatosis with a growing global prevalence. Its etiopathogenesis involves genetic, immunologic, and environmental factors. Similar to other chronic inflammatory diseases, oxidative stress plays a significant role in its pathogenesis. Squid ink polysaccharides (SIP), the primary components derived from squid ink, have demonstrated beneficial effects in terms of antioxidative properties and immune system enhancement. Nevertheless, the exact impact of SIP on specific cytokines associated with AD remains uncertain. We presented empirical data demonstrating that SIP possesses the capacity to modulate the production of epidermal-barrier-proteins, namely filaggrin (FLG) and involucrin (IVL), within keratinocytes when stimulated by tumor necrosis factor-alpha (TNF-α) and interferon gamma (IFN-γ). Additionally, SIP exhibited noteworthy anti-inflammatory properties on thymic stromal lymphopoietin (TSLP) and interleukin 8 (IL-8). Concurrently, the utilization of SIP exhibited supplementary effectiveness in alleviating AD-like cutaneous symptoms induced by 2,4-dinitrochlorobenzene, encompassing the reinstatement of the epidermal barrier, diminution of immune cell infiltration, and suppression of inflammatory cytokines in murine subjects. These in vivo outcomes were consistent with the observed reduction in TSLP levels, which was accomplished through the Piezo 1-Ca2+-NFAT1 signaling pathway. Considering these cumulative discoveries, SIP emerges as a promising therapeutic contender for the management of AD.

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“…In contrast, SOD, along with GSH-Px, is an effective ROS scavenger. Increased levels of ROS reflect the ability to resist oxidative damage [ 41 ]. In the induced POI model, the expression of oxidative stress products (ROS, T-AOC, and MDA) increased, whereas that of antioxidant products (SOD and GSH-Px) decreased.…”

Section: Discussionmentioning

confidence: 99%

Quercetin alleviates cyclophosphamide-induced premature ovarian insufficiency in mice by reducing mitochondrial oxidative stress and pyroptosis in granulosa cells

et al. 2022

View full text Add to dashboard Cite

Background Exposure to cyclophosphamide (CTX) induces premature ovarian insufficiency (POI). Quercetin is a natural flavonoid that exhibits anti-inflammatory and antioxidant properties, and its antioxidant activity is correlated with POI. However, the mechanism underlying its protective role in CTX-induced ovarian dysfunction is unclear. This study aimed to explore whether quercetin can protect ovarian reserves by activating mitochondrial biogenesis and inhibiting pyroptosis. Methods Thirty-six female C57BL/6 mice were randomly subdivided into six groups. Except for the control group, all groups were injected with 90 mg/kg CTX to establish a POI model and further treated with coenzyme 10 or various doses of quercetin. The mice were sacrificed 48 h after 10 IU pregnant mare serum gonadotropin was injected four weeks after treatments. We used enzyme-linked immunosorbent assays to detect serum hormone expression and light and transmission electron microscopy to assess ovarian tissue morphology and mitochondria. Additionally, we tested oxidant and antioxidant levels in ovarian tissues and mitochondrial function in granulosa cells (GCs). The expression of mitochondrial biogenesis and pyroptosis-related proteins and mRNA was analyzed using western blotting and RT-qPCR. Results Quercetin elevated serum anti-Müllerian hormone, estradiol, and progesterone levels, decreased serum follicle-stimulating hormone and luteinizing hormone levels, and alleviated ovarian pathology. It reduced the mitochondrial DNA content and mitochondrial membrane potential. Furthermore, it upregulated ATP levels and the mRNA and protein expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α), mitochondrial transcription factor A, and superoxide dismutase 2. In addition, it suppressed NOD-like receptor pyrin domain containing 3, caspase-1, interleukin-1β, and gasdermin D levels in the GCs of POI mice. Conclusions Quercetin protected the ovarian reserve from CTX-induced ovarian damage by reversing mitochondrial dysfunction and activating mitochondrial biogenesis via the PGC1-α pathway. Moreover, quercetin may improve ovarian functions by downregulating pyroptosis in the CTX-induced POI model. Thus, quercetin can be considered a potential agent for treating POI.

show abstract

Squid Ink Polysaccharides Protect Human Fibroblast Against Oxidative Stress by Regulating NADPH Oxidase and Connexin43

Cited by 19 publications

References 50 publications

Quercetin alleviates cyclophosphamide-induced premature ovarian insufficiency in mice by reducing mitochondrial oxidative stress and pyroptosis in granulosa cells

Quercetin alleviates cyclophosphamide-induced premature ovarian insufficiency in mice by reducing mitochondrial oxidative stress and pyroptosis in granulosa cells

Squid Ink Polysaccharides inhibit TSLP expression via the Piezo 1-Ca2+-NFAT1 signaling to ameliorate Atopic Dermatitis

Quercetin alleviates cyclophosphamide-induced premature ovarian insufficiency in mice by reducing mitochondrial oxidative stress and pyroptosis in granulosa cells

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