Ulinastatin attenuates vascular endothelial cell damage in pregnant women with severe pre-eclampsia

Abstract Ascorbic acid (AsA) therapy for sepsis is thought to have a protective effect on vascular endothelial cells, but the effect of AsA therapy on endothelial cell dysfunction over time and the appropriate timing for AsA administration to demonstrate efficacy is unclear. Septic mice, induced by cecal ligation and puncture (CLP), were examined for the effect of AsA administration (200 mg/kg) on vascular endothelial cell dysfunction at two administration timings: early group (AsA was administered immediately after CLP) and late group (AsA was administered 12 h after CLP). Survival rates were compared between the early and late administration groups, and vascular endothelial cell damage, indicated by the dihydrobiopterin/tetrahydrobiopterin ratio, serum syndecan-1, and endothelial nitric oxide synthase, as well as liver damage, were examined. The early group showed significantly improved survival compared to the non-treatment group (p < 0.05), while the late group showed no improved survival compared to the non-treatment group. Early AsA administration suppressed damage to the vascular endothelial system and liver compared to the non-treatment group. In septic mice, early AsA administration immediately after CLP may have protective effects on vascular endothelial cells, resulting in reduced organ dysfunction and improved survival.

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miR-4286/TGF-β1/Smad3-Negative Feedback Loop Ameliorated Vascular Endothelial Cell Damage by Attenuating Apoptosis and Inflammatory Response

Journal of Cardiovascular Pharmacology ◽

10.1097/fjc.0000000000000813 ◽

2020 ◽

Vol 75 (5) ◽

pp. 446-454

Author(s):

Zhiyu He ◽

Hao Xue ◽

Peiying Liu ◽

Dunzheng Han ◽

Lingling Xu ◽

...

Keyword(s):

Endothelial Cell ◽

Inflammatory Response ◽

Negative Feedback ◽

Feedback Loop ◽

Cell Damage ◽

Vascular Endothelial Cell ◽

Negative Feedback Loop ◽

Vascular Endothelial ◽

Endothelial Cell Damage ◽

Tgf Β1

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Study of the Pharmacological Effect of the Bile Salt, Sodium Scymnol Sulfate, from Rhizoprionodon acutus. III. Protective Effect of Scymnol against Vascular Endothelial Cell Damage in a Rat Peripheral Arterial Occlusion Model.

Biological and Pharmaceutical Bulletin ◽

10.1248/bpb.22.822 ◽

1999 ◽

Vol 22 (8) ◽

pp. 822-827 ◽

Cited By ~ 5

Author(s):

Hitosi ISHIDA ◽

Hidetoshi NAKAYASU ◽

Haruo NUKAYA ◽

Kunirou TSUJI

Keyword(s):

Endothelial Cell ◽

Protective Effect ◽

Bile Salt ◽

Cell Damage ◽

Vascular Endothelial Cell ◽

Arterial Occlusion ◽

Vascular Endothelial ◽

Endothelial Cell Damage ◽

Occlusion Model ◽

Peripheral Arterial

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SPARC (secreted protein acidic and rich in cysteine) knockdown protects mice from acute liver injury by reducing vascular endothelial cell damage

Gene Therapy ◽

10.1038/gt.2014.102 ◽

2014 ◽

Vol 22 (1) ◽

pp. 9-19 ◽

Cited By ~ 11

Author(s):

E Peixoto ◽

C Atorrasagasti ◽

J B Aquino ◽

R Militello ◽

J Bayo ◽

...

Keyword(s):

Endothelial Cell ◽

Liver Injury ◽

Acute Liver Injury ◽

Cell Damage ◽

Vascular Endothelial Cell ◽

Secreted Protein ◽

Vascular Endothelial ◽

Endothelial Cell Damage

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Expression of DUSP12 Reduces Lung Vascular Endothelial Cell Damage in a Murine Model of Lipopolysaccharide-Induced Acute Lung Injury via the Apoptosis Signal-Regulating Kinase 1 (ASK1)-Jun N-Terminal Kinase Activation (JNK) Pathway

Medical Science Monitor ◽

10.12659/msm.930429 ◽

2021 ◽

Vol 27 ◽

Author(s):

Zhao Hui ◽

Huang Jie ◽

Guo-Hua Fan

Keyword(s):

Acute Lung Injury ◽

Endothelial Cell ◽

Lung Injury ◽

Murine Model ◽

Cell Damage ◽

Vascular Endothelial Cell ◽

Vascular Endothelial ◽

Endothelial Cell Damage ◽

Jnk Pathway ◽

Kinase Activation

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Can Bioactive Lipid Arachidonic Acid Prevent and Ameliorate COVID-19?

Medicina ◽

10.3390/medicina56090418 ◽

2020 ◽

Vol 56 (9) ◽

pp. 418 ◽

Cited By ~ 1

Author(s):

Undurti N. Das

Keyword(s):

Arachidonic Acid ◽

Endothelial Cell ◽

Cell Damage ◽

Vascular Endothelial Cell ◽

M2 Macrophage ◽

Vascular Endothelial ◽

Endothelial Cell Damage ◽

Lipoxin A4 ◽

Inflammation Resolution ◽

Resolution Processes

It is proposed that the bioactive lipid, arachidonic acid (AA, 20:4 n-6), can inactivate severe acute respiratory syndrome(SARS-CoV-2), facilitate M1 and M2 macrophage generation, suppress inflammation, prevent vascular endothelial cell damage, and regulate inflammation resolution processes based on the timely formation of prostaglandin E2 (PGE2) and lipoxin A4 (LXA4) based on the context. Thus, AA may be useful both to prevent and manage coronavrus disease-2019(COVID-19).

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Effect of baicalin on gestational hypertension-induced vascular endothelial cell damage

Journal of International Medical Research ◽

10.1177/0300060520934288 ◽

2020 ◽

Vol 48 (10) ◽

pp. 030006052093428

Author(s):

Yang Liu ◽

Miao Xiong ◽

Fangfang Zhou ◽

Nana Shi ◽

Yunbin Jia

Keyword(s):

Endothelial Cell ◽

Cell Damage ◽

Vascular Endothelial Cell ◽

Vascular Endothelial ◽

Pregnancy Induced Hypertension ◽

Hypertensive Rats ◽

Endothelial Cell Damage ◽

Pregnant Rat ◽

Induced Hypertension ◽

Β Hcg

Objective Baicalin is a compound extracted from the dried root of Scutellaria baicalensis Georgi. Studies have shown that baicalin has a protective effect on vascular endothelial cells, but whether baicalin could alleviate ascular endothelial cell damage in pregnancy-induced hypertensive patients remains unknown. Materials and methods We established a hypertensive pregnant rat model to study vascular endothelial injury during pregnancy-induced hypertension. Plasma epoprostenol (PGI-2), thromboxane A2 (Txa-2), β-human chorionic gonadotropin (β-HCG), and estrogen levels in rats were detected using ELISA. Vascular endothelial growth factor (VEGF), endothelial nitric oxide synthase (eNOS), and C-reactive protein (CRP) expression were detected using western blotting and quantitative PCR (q-PCR). Results Results showed that baicalin alleviated symptoms of pregnancy-induced hypertension. CRP, Txa-2, and β-HCG expression were significantly upregulated, while VEGF, eNOS, PGI-2, and estrogen expression was decreased in plasma and placental tissues of hypertensive rats. However, the levels of these injury indicators were significantly decreased after baicalin therapy, while the expression of protective indicators was significantly increased. Conclusion Baicalin reversed vascular endothelial cell injury in pregnant hypertensive rats by promoting VEGF, eNOS, PGI-2, and estrogen expression.

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