Escin suppresses HMGB1‐induced overexpression of aquaporin‐1 and increased permeability in endothelial cells

Chen, Changjun; Wang, Songgang; Chen, Jiying; Liu, Xiaolin; Zhang, Mengchen; Wang, Xi; Xu, Weihua; Zhang, Yayun; Li, Hao; Pan, Xin; Si, Meng

doi:10.1002/2211-5463.12622

Cited by 17 publications

(12 citation statements)

References 30 publications

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“…Analogous to our results, Mohamed et al [2019] demonstrated that CoQ10 decreased HMGB1 expression in a rat model of lung fibrosis. Additionally, AES administration had an anti-inflammatory effect via suppression of HMGB1 in different inflammation-related disease models [Cheng et al, 2015;Chen et al, 2019]. Importantly, our data also show that combined pretreatment of animals with CoQ10 and AES restricted the HMGB1 expression compared to separate drugs.…”

Section: Discussionsupporting

confidence: 59%

Pretreatment with Coenzyme Q10 Combined with Aescin Protects against Sepsis-Induced Acute Lung Injury

Ali

Ahmed

Eltrawy

et al. 2021

Cells Tissues Organs

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Sepsis-associated acute lung injury (ALI) is a critical condition characterized by severe inflammatory response and mitochondrial dysfunction. Coenzyme Q10 (CoQ10) and aescin (AES) are well-known for their anti-inflammatory activities. However, their effects on lipopolysaccharide (LPS)-induced lung injury have not been explored yet. Here, we asked whether combined pretreatment with CoQ10 and AES synergistically prevents LPS-induced lung injury. Fifty male rats were randomized into 5 groups: (1) control; (2) LPS-treated, rats received a single i.p. injection of LPS (8 mg/kg); (3) CoQ10-pretreated, (4) AES-pretreated, or (5) combined-pretreated; animals received CoQ10 (100 mg/kg), AES (5 mg/kg), or both orally for 7 days before LPS injection. Combined CoQ10 and AES pretreatment significantly reduced lung injury markers; 52.42% reduction in serum C-reactive protein (CRP), 53.69% in alkaline phosphatase (ALKP) and 60.26% in lactate dehydrogenase (LDH) activities versus 44.58, 37.38, and 48.6% in CoQ10 and 33.81, 34.43, and 39.29% in AES-pretreated groups, respectively. Meanwhile, combination therapy significantly reduced interleukin (IL)-1β and tumor necrosis factor (TNF)-α expressions compared to monotherapy (p < 0.05). Additionally, combination therapy prevented LPS-induced histological and mitochondrial abnormalities greater than separate drugs. Western blotting indicated that combination therapy significantly suppressed nucleotide-binding oligomerization domain (NOD)-like receptors-3 (NLRP-3) inflammasome compared to separate drugs (p < 0.05). Further, combination therapy significantly decreased the expression of signaling cascades, p38 mitogen-activated protein kinases (p38 MAPK), nuclear factor kappa B (NF-κB)-p65, and extracellular-regulated kinases 1/2 (ERK1/2) versus monotherapy (p < 0.05). Interestingly, combined pretreatment significantly downregulated high mobility group box-1 (HMGB1) by 72.93%, and toll-like receptor 4 (TLR4) by −0.93-fold versus 61.92%, −0.83-fold in CoQ10 and 38.67%, −0.70-fold in AES pretreatment, respectively. Our results showed for the first time that the enhanced anti-inflammatory effect of combined CoQ10 and AES pretreatment prevented LPS-induced ALI via suppression of NLRP-3 inflammasome through regulation of HMGB1/TLR4 signaling pathway and mitochondrial stabilization.

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Section: Discussionsupporting

confidence: 59%

Pretreatment with Coenzyme Q10 Combined with Aescin Protects against Sepsis-Induced Acute Lung Injury

Ali

Ahmed

Eltrawy

et al. 2021

Cells Tissues Organs

View full text Add to dashboard Cite

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“…Certain drugs are reported to inhibit HMGB1, including TNF-alpha inhibitors, corticosteroids, chloroquine, statins, and anticancer drugs cisplatine, daunomycine, methothrexate, which show their action towards humoral, cellular immune response or both. Antiagregant clopidogrel, anticoagulants heparin, thrombomodulin, danaparoid, antithrombin and activated protein C are also demonstrated to inhibit HMGB1 expression, release or activity [2][3][4][5][6][7][8][9][10][11][12][13][14]24]. Though the number of patients in our cohort is limited, we observed a very good response to corticosteroids in patients who have high HMGB1 levels.…”

Section: Discussionmentioning

confidence: 97%

Value of Extracellular High Mobility Group Box 1 (HMGB1) in the Clinical Context of Immune Thrombocytopenia

et al. 2019

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Introduction: High mobility group box 1 protein (HMGB1) is a non-histone chromosomal protein with dual activity. First within the nucleus, binds to DNA and acts as a regulator and second, outside the cell, interacts with receptors for inflammation as a signal molecule. We aimed to investigate and contribute to the value of extracellular HMGB1 in clinical context of ITP and to flourish future clinical directions to this biomarker. Methods: 50 newly diagnosed and treatment naive patients with ITP and 30 healthy controls were enrolled in our study. Results: Age or gender were not related with HMGB1 levels in patients and controls. Platelet levels were significantly related with HMGB1. Especially in patients with platelet counts below 30.000/mm3 highest levels of HMGB1 were observed. Regarding clinical presentation, bleeding was related with low platelet counts and high HMGB1 levels. Response to corticosteroids was observed to be better in patients with high HMGB1 levels. Conclusion: As a sample of autoinflammatory disorders, we observed a relation with extracellular HMGB1 levels and platelet levels in ITP patients. Corticosteroid response and HMGB1 relation supports the assumption of the value of HMGB1 as a potential surrogate of inflammation. This view should be evaluated with larger scale studies.

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“…Albumin is synthesized and secreted by liver cells, which can maintain nutrition and osmotic pressure of the body, transport many insoluble small molecules of organic matter and inorganic ions, and participate in the inflammation process. Inflammatory response can induce barrier dysfunction, resulting in endothelial cell and albumin hyperpermeability and increased tissue oedema ( Chen et al, 2019 ). Serum albumin, as an anti-inflammatory protein, has a protective anti-inflammatory effect during acute inflammation ( China et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

Association between fibrinogen/albumin ratio and severity of coronary artery calcification in patients with chronic kidney disease: a retrospective study

Zhu

Tao

Zhang

et al. 2022

PeerJ

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Aim Previous studies have shown that the fibrinogen to albumin ratio (FAR) is closely related to the severity and prognosis of coronary atherosclerosis. In this study, we sought to evaluate the association between FAR and the degree of coronary artery calcification (CAC) in patients with chronic kidney disease (CKD). Methods In this retrospective study, 218 patients with CKD were stratified into low, medium and high FAR groups according to the tertiles of the FAR values. The CAC scores, clinical information and laboratory test results of the three FAR groups were compared. To explore the relationship between FAR and CAC we conducted binary logistic regression and correlation analyses. Results In the low FAR group, the CAC scores were significantly lower than those in the medium and high FAR groups (P < 0.001). There was a significant correlation between the FAR and CAC scores (r = 0.510, P < 0.001). The FAR was an independent predictor of CAC (OR = 1.106, 95% CI [1.004–1.218], P = 0.042). Conclusion In patients with CKD, the FAR can be considered as an effective predictor of CAC.

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Escin suppresses HMGB1‐induced overexpression of aquaporin‐1 and increased permeability in endothelial cells

Cited by 17 publications

References 30 publications

Pretreatment with Coenzyme Q10 Combined with Aescin Protects against Sepsis-Induced Acute Lung Injury

Pretreatment with Coenzyme Q10 Combined with Aescin Protects against Sepsis-Induced Acute Lung Injury

Value of Extracellular High Mobility Group Box 1 (HMGB1) in the Clinical Context of Immune Thrombocytopenia

Association between fibrinogen/albumin ratio and severity of coronary artery calcification in patients with chronic kidney disease: a retrospective study

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