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Uvaol Inhibits Inflammatory Response and Prevents Lipopolysaccharide-Induced Acute Lung Injury in Mice (Record no. 130091)

MARC details
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008 - FIXED-LENGTH DATA ELEMENTS--GENERAL INFORMATION
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100 ## - MAIN ENTRY--PERSONAL NAME
Personal name Yubo Shi1
245 ## - TITLE STATEMENT
Title Uvaol Inhibits Inflammatory Response and Prevents Lipopolysaccharide-Induced Acute Lung Injury in Mice
300 ## - PHYSICAL DESCRIPTION
Extent P271-279
520 ## - SUMMARY, ETC.
Summary, etc. biblio.abstract Sepsis is a clinical disease characterized by systemic inflammatory reactions following infection that can lead to multiorgan failure. Acute Lung Injury (ALI) is a common ailment with increased morbidity and fatality rates worldwide. Objectives: The present investigation was planned to investigate the salutary activities of uvaol against Lipopolysaccharide (LPS)-exposed ALI in mice. Materials and Methods: The 5 mg/kg of LPS was exposed to the mice for 3 days through the intra-tracheal route to initiate the ALI, and 5 and 10 mg/kg, respectively, of uvaol were administered orally for 3 days the LPS challenge. The mice were scarified under anesthesia, lungs were excised, and wet and dry weights were weighed accurately. All the biochemical parameters, including apoptosis, inflammation, and oxidative stress marker levels, were assessed using the respective assay kits. Results: The uvaol (5 and 10 mg/kg) treatment effectively diminished pulmonary edema, total protein, and LDH activity in the ALI mice. The MDA was reduced, and the GSH and SOD levels were increased by the uvaol. The uvaol effectively reduced the inflammatory cytokines and infiltrations in the ALI mice. The PGE-2, iNOS, and COX-2 levels in the BALF of ALI mice were effectively reduced by the uvaol. The Bax and caspase-3 expression was reduced, and the Bcl-2 was elevated by the uvaol. The outcomes of histopathological analysis also supported the therapeutic potential of uvaol against ALI. Conclusion: In conclusion, the outcomes of the current exploration highlighted that uvaol considerably prevented the LPS-exposed ALI in mice via its antioxidant and anti-inflammatory effects. Hence, it can be concluded that uvaol can be employed in the treatment of ALI in the future
654 ## - SUBJECT ADDED ENTRY--FACETED TOPICAL TERMS
Subject <a href=" Lipopolysaccharide"> Lipopolysaccharide</a>
-- <a href=" Cytokines"> Cytokines</a>
-- <a href=" Apoptosis"> Apoptosis</a>
-- <a href=" Uvaol"> Uvaol</a>
-- <a href=" Lung edema"> Lung edema</a>
-- <a href=" Sepsis"> Sepsis</a>
700 ## - ADDED ENTRY--PERSONAL NAME
Personal name Airu Wang2
-- Hua Jiang3
773 0# - HOST ITEM ENTRY
Host Biblionumber 125266
Host Itemnumber 109601
Place, publisher, and date of publication Banglore Association of Pharmaceutical Tearchers of India
Title Indian Journal of Pharmaceutical Education and Research
International Standard Serial Number 0019-5464
942 ## - ADDED ENTRY ELEMENTS (KOHA)
Koha item type Journal Article
773 0# - HOST ITEM ENTRY
-- JP44
942 ## - ADDED ENTRY ELEMENTS (KOHA)
-- ddc
Holdings
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    Dewey Decimal Classification     SNDT Juhu SNDT Juhu 11/11/2024   JP44.29 11/11/2024 11/11/2024 Journal Article