About: Protective Effect and Mechanism of Alprostadil in Acute Respiratory Distress Syndrome Induced by Oleic Acid in Rats

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About: Protective Effect and Mechanism of Alprostadil in Acute Respiratory Distress Syndrome Induced by Oleic Acid in Rats Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Protective Effect and Mechanism of Alprostadil in Acute Respiratory Distress Syndrome Induced by Oleic Acid in Rats
Creator	Ye, Jing Cui, Qingsong Jiang, Jingzhi Jin, Minggen Li, Liangchang Li, Yingxiu Piao, Yihua Wang, Chongyang Xu, Huixian Yan, Guanghai Yan, Xiujuan Choi, Yun
Source	PMC
abstract	BACKGROUND: This study investigated the role and mechanism of alprostadil in acute respiratory distress syndrome (ARDS) induced by oleic acid (OA) in rats. MATERIAL/METHODS: Sprague-Dawley rats were randomly divided into control, OA model, and OA + Alprostadil (2.5, 5, and 10 μg/kg, respectively) groups. The ARDS model was induced by femoral vein injection of OA, and alprostadil was administrated immediately. Lung injury was evaluated by lung wet-dry weight ratio (W/D) and histological analyses. Expressions of ACE, inflammatory mediators, apoptotic-related proteins, and proteins in the MAPKs and NF-κB signaling pathways were determined by Western blot or immunohistochemical staining. RESULTS: Compared with the control group, the OA model group had significantly increased W/D, lung injury score, and collagen deposition at 3 h after OA injection. However, alprostadil (10 μg/kg) treatment significantly reduced OA-induced elevation of these indicators. Additionally, OA-induced expression of TNF-α and IL-1β were suppressed by alprostadil. The OA-induced activation of nuclear factor (NF) κB p65 was also reduced by alprostadil. Furthermore, we found that Alprostadil had an inhibitory effect on the phosphorylation of JNK, ERK1/2, and p38 MAPKs. Alprostadil inhibited Bax but increased Bcl-2, indicating a suppressive role in apoptosis. Remarkably increased expression of ACE in the OA model group was observed, which was decreased by alprostadil. CONCLUSIONS: Alprostadil has a protective effect on ARDS induced by OA in rats, possibly through inhibiting apoptosis, suppressing the activation of MAPKs and NF-κB signaling pathways, and decreasing ACE protein expression. Therefore, the use of alprostadil in clinical ARDS treatment is promising.
has issue date	2018-10-08(xsd:dateTime)
bibo:doi	10.12659/msm.909678
bibo:pmid	30296789
has license	cc-by-nc-nd
sha1sum (hex)	41199e837e1c706b7a8a1a8a0970856974235566
schema:url	https://doi.org/10.12659/msm.909678
resource representing a document's title	Protective Effect and Mechanism of Alprostadil in Acute Respiratory Distress Syndrome Induced by Oleic Acid in Rats
has PubMed Central identifier	PMC6190919
has PubMed identifier	30296789
schema:publication	Med Sci Monit
resource representing a document's body	covid:41199e837e1c706b7a8a1a8a0970856974235566#body_text
is schema:about of	named entity 'INDUCED' named entity 'OLEIC ACID' named entity 'STUDY' named entity 'ROLE' named entity 'RATS' named entity 'INVESTIGATED' named entity 'ACUTE RESPIRATORY DISTRESS SYNDROME' named entity 'ALPROSTADIL' named entity 'ACUTE RESPIRATORY DISTRESS SYNDROME' named entity 'PROTECTIVE EFFECT' named entity 'MECHANISM' named entity 'OLEIC ACID' named entity 'INDUCED' named entity 'MECHANISM' named entity 'RATS' named entity 'ALPROSTADIL' covid:arg/41199e837e1c706b7a8a1a8a0970856974235566 named entity 'acid' named entity 'Oleic Acid' named entity 'Jilin' named entity 'ACE' named entity 'Alprostadil' named entity 'TNF-a' named entity 'oleic acid' named entity 'TNF-a' named entity 'alveolar' named entity 'Animal Research' named entity 'animal models' named entity 'China' named entity 'Alprostadil' named entity 'ACE' named entity 'NF-kB' named entity 'Bcl-2' named entity 'ARDS' named entity 'phosphorylation' named entity 'salt balance' named entity 'alveolar' named entity 'fibrosis' named entity 'leukocyte' named entity 'up-regulated' named entity 'lung edema' named entity 'pneumonia' named entity 'hemorrhage' named entity 'SPSS' named entity 'ACE' named entity 'lung tissue' named entity 'ethanol' named entity 'lung injury' named entity 'Bcl-2' named entity 'Berlin' named entity 'fibrosis' named entity 'fibrosis' named entity 'deionized water' named entity 'administrated' named entity 'AT1 receptor' named entity 'TNF-a' named entity 'vasoconstriction' named entity 'ACE' named entity 'Reagent' named entity 'neutrophils' named entity 'serum' named entity 'Masson's trichrome' named entity 'microsphere' named entity 'positive staining' named entity 'bronchial airways' named entity 'alprostadil' named entity 'pulmonary circulation' named entity 'ARDS' named entity 'Laboratory Animals' named entity 'Bcl-2 family'

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