Protocatechuic acid attenuates lipopolysaccharide‐induced septic lung injury in mice: The possible role through suppressing oxidative stress, inflammation and apoptosis. Issue 10 (2nd September 2021)

• Record Type: Journal Article
• Authors: Alsharif, Khalaf F.; Almalki, Abdulraheem Ali; Alsanie, Walaa F.; Alzahrani, Khalid J.; Kabrah, Saeed M.; Elshopakey, Gehad E.; Alghamdi, Abdullah A. A.; Lokman, Maha S.; Sberi, Hassan Al; Bauomy, Amira A.; Albrakati, Ashraf; Ramadan, Shimaa S.; Kassab, Rami B.; Abdel Moneim, Ahmed E.; Salem, Fatma Elzahraa H.
• Is Part Of: Journal of food biochemistry. Volume 45:Issue 10(2021)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2021-09-02
• Subjects: apoptotic markers -- inflammatory biomarkers -- lipopolysaccharide -- oxidative damage -- protocatechuic acid -- sepsis; Food -- Analysis -- Periodicals; Food -- Composition -- Periodicals; Biochemistry -- Periodicals; 664.024
• DOI: 10.1111/jfbc.13915
• Languages: English
• ISSNs: 0145-8884

Abstract

Abstract: Here, we investigated the protective efficacy of protocatechuic acid (PCA) against lipopolysaccharide (LPS)‐induced septic lung injury. Eighty‐two male Balb/c mice were divided into six groups: control, PCA30 (30 mg/kg), LPS (10 mg/kg), PCA10‐LPS, PCA20‐LPS, and PCA30‐LPS treated with 10, 20 and 30 mg/kg PCA, respectively, for seven days before intraperitoneal LPS injection. PCA pre‐treatment, especially at higher dose, significantly reduced LPS‐induced lung tissue injury as indicated by increased heat shock protein 70 and antioxidant molecules (reduced glutathione, superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase) accompanied by lower oxidative stress indices (malondialdehyde and nitric oxide). PCA administration decreased inflammatory mediators including myeloperoxidase, nuclear factor kappa B (NF‐κB p65), and pro‐inflammatory cytokines, and prevented the development of apoptotic events in the lung tissue. At the molecular level, PCA downregulated mRNA expression of nitric oxide synthase 2, C/EBP homologous protein, and high mobility group box1 in the lungs of all PCA‐LPS treated mice. Thus, PCA‐pre‐treatment effectively counteracted sepsis‐induced acute lung injury in vivo by promoting and antioxidant status, while inhibiting inflammation and apoptosis. Practical implications: Sepsis‐mediated organ dysfunction and high mortality is aggravated by acute lung injury (ALI). Therefore, new therapeutic approaches are needed to encounter sepsis‐mediated ALI. Protocatechuic acid (PCA) is a naturally occurring phenolic acid with various biological and pharmacological activities. PCA is abundant in edible plants including Allium cepa L., Oryza sativa L., Hibiscus sabdariffa, Prunus domestica L., and Eucommia ulmoides . In this investigation we studied the potential protective role of pure PCA (10, 20 and 30 mg/kg) on LPS‐mediated septic lung injury in mice through examining oxidative challenge, inflammatory response, apoptotic events and histopathological changes in addition to evaluating the levels and mRNA expression of heat shock protein 70, C/EBP homologous protein and high mobility group box1 in the lung tissue. The recorded results showed that PCA pre‐administration was able to significantly abrogate the damages in the lung tissue associated septic response. This protective effect comes from its strong antioxidant, anti‐inflammatory, and anti‐apoptotic activities, suggesting that PCA may be applied to alleviate ALI associated with the development of sepsis. Abstract : Protocatechuic acid (PCA) abrogated oxidative insults associated with lipopolysaccharide (LPS)‐mediated acute lung injury through enhancing antioxidant molecules and inhibiting pro‐oxidants. PCA inhibited inflammatory response accompanied septic shock in response to LPS injection. PCA protected lung tissue and prevented cell lose through inhibiting apoptotic events following LPS‐induced sepsis.