Epigallocatechin-3-gallate Ameliorates Seawater Aspiration-Induced Acute Lung Injury via Regulating Inflammatory Cytokines and Inhibiting JAK/STAT1 Pathway in Rats

Liu, Wei; Dong, Minyue; Bo, Liyan; Li, Congcong; Liu, Qingqing; Li, Yanyan; Ma, Li; Xie, Youhua; Fu, Enqing; Mu, Deguang; Pan, Lei; Jin, Fang; Li, Zhichao

doi:10.1155/2014/612593

Cited by 38 publications

(42 citation statements)

References 26 publications

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“…The hyperosmolar seawater has direct effect on the lung epithelial cells and causes the infiltration of inflammation cells into the alveolar spaces and releases various molecules, leading to lung edema and deterioration of gas exchange [3][4][5][6]15]. Proinflammatory cytokines, such as TNF-α and IL-6, are critical for initiating, amplifying, and perpetuating organ injury [5,6].…”

Section: Discussionmentioning

confidence: 99%

“…Proinflammatory cytokines, such as TNF-α and IL-6, are critical for initiating, amplifying, and perpetuating organ injury [5,6]. On the other hand, reactive oxygen species (ROS) overproduction is another feature of ALI, which is involved in the microvascular endothelial cell injury and the pathology of ALI [14,16,17].…”

Section: Discussionmentioning

confidence: 99%

“…These pathological processes in turn can lead to alveolar epithelial-endothelial capillary barrier disruption, pulmonary edema, and severe refractory hypoxemia. Although many agents have been shown to attenuate seawater aspiration-induced ALI [4][5][6], alternative agents are needed to prevent or treat seawater aspiration-induced ALI.…”

Section: Discussionmentioning

confidence: 99%

“…Seawater aspiration represents one of the most important causes of acute lung injury (ALI), which is characterized by pulmonary edema and severe refractory hypoxemia [1][2][3][4]. In addition, the increased alveolar-capillary permeability caused by seawater aspiration allows the inflammatory cells infiltrate into the alveolar spaces and releases several molecules, such as pro-inflammatory cytokines and reactive oxygen species, leading to further pulmonary edema and deterioration of gas exchange [3,5,6]. Thus, agents that inhibit the overwhelming inflammatory responses and oxidative stress process may provide a therapeutic option for the treatment of seawater aspiration-induced ALI.…”

Section: Introductionmentioning

confidence: 99%

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Erythropoietin Pretreatment Attenuates Seawater Aspiration-Induced Acute Lung Injury in Rats

Tong

Tan

et al. 2015

Inflammation

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Seawater drowning-induced acute lung injury (ALI) is a serious clinical condition characterized by increased alveolar-capillary permeability, excessive inflammatory responses, and refractory hypoxemia. However, current therapeutic options are largely supportive; thus, it is of great interest to search for alternative agents to treat seawater aspiration-induced ALI. Erythropoietin (EPO) is a multifunctional agent with antiinflammatory, antioxidative, and antiapoptotic properties. However, the effects of EPO on seawater aspiration-induced ALI remain unclear. In the present study, male rats were randomly assigned to the naive group, normal saline group, seawater group, or seawater + EPO group. EPO was administered intraperitoneally at 48 and 24 h before seawater aspiration. Arterial blood gas analysis was performed with a gas analyzer at baseline, 30 min, 1 h, 4 h, and 24 h after seawater aspiration, respectively. Histological scores, computed tomography scan, nuclear factor kappa B p65, inducible nitric oxide synthase, caspase-3, tumor necrosis factor-alpha, interleukin (IL)-1β, IL-6, IL-10, wet-to-dry weight ratio, myeloperoxidase activity, malondialdehyde, and superoxide dismutase in the lung were determined 30 min after seawater aspiration. Our results showed that EPO pretreatment alleviated seawater aspiration-induced ALI, as indicated by increased arterial partial oxygen tension and decreased lung histological scores. Furthermore, EPO pretreatment attenuated seawater aspiration-induced increase in the expressions of pulmonary nuclear factor kappa B p65, inducible nitric oxide synthase, caspase-3, tumor necrosis factor-alpha, IL-1β, myeloperoxidase activity, and malondialdehyde when compared with the seawater group. Collectively, our study suggested that EPO pretreatment attenuates seawater aspiration-induced ALI by down-regulation of pulmonary pro-inflammatory cytokines, oxidative stress, and apoptosis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Erythropoietin Pretreatment Attenuates Seawater Aspiration-Induced Acute Lung Injury in Rats

Tong

Tan

et al. 2015

Inflammation

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“…It is has been widely consumed for three millennia as a beverage and is known to have medicinal properties. Recent work with EGCG, and related catechins, has shown it has powerful anti-oxidant properties 1 and displays anti-tumor, 2 anti-inflammatory, 3,4 antikeloid scar formation, 5 alters apoptosis, [5][6][7][8] anti-metastatic, 9,10 and anti-atherogenic 11 activity both in vitro and in vivo settings. EGCG also has been demonstrated to inhibit growth of microbes such as Acinetobacter baumannii, 12 Bordetella pertussis, 13 Helicobacter pylori, 14,15 Porphyromonas gingivalis, 16,17 Staphylococcus aureus and Eschericia coli 18 and Salmonella typhimurium.…”

Section: Introductionmentioning

confidence: 99%

The Effects of (-)-Epigallocatechin-3-Galate on Wound Closure and Infections in Mice

Osterburg¹,

Yamaguchi²,

Robinson³

et al. 2015

Surg Res Open J

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In this study, we investigated the effects of (-)-epigallocatechin-3-gallate (EGCG) on wound healing both in vitro and in vivo with and without infection. EGCG has antimicrobial properties and could be useful as a topical agent to prevent and/or treat wound infections. Normal fibroblasts were isolated from the dermis of C57BL/6 mice and cultured with 0, 0.001 to 0.400 mg/ml of EGCG. In vitro assays demonstrated that migration, proliferation, and apoptosis were inhibited at EGCG concentrations of 0.100-0.400 mg/ml. Expression of α-smooth muscle actin (α-SMA) was also reduced. In vivo experiments measured closure/contraction of full-thickness dorsal wounds that were treated with 0, 0.3, 3.0, and 30.0 mg/ml of EGCG every 24 hours. Macrophages (F4/80), neutrophils (Ly-6G) and myofibroblasts (α-SMA) were assessed at 48 and 168 hours. By 168 hours there was a significant reduction in presence with the 30 mg/ml dose vs. 0.3 and 3.0 mg/ml (p<0.009, p<0.006, respectively). The percentage of wound closure at one week in EGCG treated wounds was 87.87% (0.03 mg), 85.23% (0.3 mg) and 40.06% (30 mg/ml) compared to controls. Reduced quantities of α-SMA myofibroblasts were observed in the 3 mg EGCG treatment group compared to controls at 168 hours. We previously demonstrated that EGCG has antimicrobial properties (MIC 50 ~0.3 mg/ml). This data suggests that EGCG could potentially be applied to the wound surface as an antimicrobial without negatively influencing healing. To this end we applied EGCG (10 mg/ml) to a model of an infected traumatic wound. EGCG treatment significantly reduced bacterial load after one and two dose regimens.

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Flavonoids as potential phytotherapeutics to combat cytokine storm in SARS‐CoV‐2

Gour

Manhas

Bag

et al. 2021

Phytotherapy Research

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Emergence of severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2) infection, COVID‐19, has become the global panic since December 2019, which urges the global healthcare professionals to identify novel therapeutics to counteract this pandemic. So far, there is no approved treatment available to control this public health issue; however, a few antiviral agents and repurposed drugs support the patients under medical supervision by compromising their adverse effects, especially in emergency conditions. Only a few vaccines have been approved to date. In this context, several plant natural products‐based research studies are evidenced to play a crucial role in immunomodulation that can prevent the chances of infection as well as combat the cytokine release storm (CRS) generated during COVID‐19 infection. In this present review, we have focused on flavonoids, especially epicatechin, epigallocatechin gallate, hesperidin, naringenin, quercetin, rutin, luteolin, baicalin, diosmin, ge nistein, biochanin A, and silymarin, which can counteract the virus‐mediated elevated levels of inflammatory cytokines leading to multiple organ failure. In addition, a comprehensive discussion on available in silico, in vitro, and in vivo findings with critical analysis has also been evaluated, which might pave the way for further development of phytotherapeutics to identify the potential lead candidatetoward effective and safe management of the SARS‐CoV‐2 disease.

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Epigallocatechin-3-gallate Ameliorates Seawater Aspiration-Induced Acute Lung Injury via Regulating Inflammatory Cytokines and Inhibiting JAK/STAT1 Pathway in Rats

Cited by 38 publications

References 26 publications

Erythropoietin Pretreatment Attenuates Seawater Aspiration-Induced Acute Lung Injury in Rats

Erythropoietin Pretreatment Attenuates Seawater Aspiration-Induced Acute Lung Injury in Rats

The Effects of (-)-Epigallocatechin-3-Galate on Wound Closure and Infections in Mice

Flavonoids as potential phytotherapeutics to combat cytokine storm in SARS‐CoV‐2

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