The effect of captopril on lipopolysaccharide-induced lung inflammation

Boskabadi, Javad; Mokhtari‐Zaer, Amin; Abareshi, Azam; Khazdair, Mohammad Reza; Emami, Bahman; Roshan, Nama Mohammadian; Hosseini, Mahmoud; Boskabady, Mohammad Hossein

doi:10.1080/01902148.2018.1473530

Cited by 18 publications

(8 citation statements)

References 37 publications

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“…Furthermore, LPS decreased the IL-4 level but increased IFN-c, TGF-β1, and PGE2 levels in the BALF. Moreover, pathological insults of the lung such as lung inflammation, epithelial damage, emphysema, and fibrosis confirmed LPSinduced lung injury in the current study which was also shown in the previous studies [8,10].…”

Section: Discussionsupporting

confidence: 91%

“…In the LPS-administered animals, decreased lymphocytes percentage was due to increased total WBC count. In fact, increased absolute lymphocytes count was demonstrated in previous studies [8,10].…”

Section: Discussionsupporting

confidence: 50%

“…A previous study also showed systemic inflammation caused by the release of inflammatory cytokines following i.p. injection of LPS [8]. It was shown that LPS induced 1 responses (IFN-c) and inhibited 2 responses (IL-4) through the toll-like receptor 4-(TLR4-) dependent pathway; also, LPS increased BALF levels of PGE2 and TGF-β1 [8].…”

Section: Discussionmentioning

confidence: 99%

“…Our previous studies showed that intraperitoneal (i.p.) administration of LPS in the rats increased total and differential WBC count, induced oxidative damage by increasing the MDA level and decreasing antioxidant markers, and led to a 1/ 2 imbalance in the blood and the BALF [7][8][9][10]. erefore, reducing oxidative injury and suppression of the inflammatory process could ameliorate LPS-induced tissue damage including lung injury.…”

Section: Introductionmentioning

confidence: 99%

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Thymoquinone Ameliorates Lung Inflammation and Pathological Changes Observed in Lipopolysaccharide-Induced Lung Injury

Khazdair

Bargi

Saadat

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Anti-inflammatory, antioxidant, and immunomodulatory effects of thymoquinone (TQ) have been shown. The effects of TQ on lipopolysaccharide- (LPS-) induced inflammation and pathological changes in rats’ lung were investigated in this study. Four groups of rats included (1) control (saline treated); (2) LPS (treated with 1 mg/kg/day i.p. for two weeks); and (3 and 4) 5 or 10 mg/kg TQ i.p. 30 min prior to LPS administration. Total and differential WBC counts in the blood and bronchoalveolar fluid (BALF), TGF-β1, INF-γ, PGE2, and IL-4 levels in the BALF and pathological changes of the lung were evaluated. Total WBC count and eosinophil, neutrophil, and monocyte percentage were increased, but the lymphocyte percentage was reduced in the blood and BALF. The BALF levels of PGE2, TGF-β1, and INF-γ were also increased, but IL-4 level was reduced due to LPS administration. LPS also induced pathological insults in the lung of rats ( P < 0.05 to P < 0.001 for all changes in LPS-exposed animals). Treatment with TQ showed a significant improvement in all changes induced by LPS ( P < 0.05 to P < 0.05 ). TQ showed a protective effect on LPS-induced lung inflammation and pathological changes in rats which suggested a therapeutic potential for TQ on lung injury.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 50%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Thymoquinone Ameliorates Lung Inflammation and Pathological Changes Observed in Lipopolysaccharide-Induced Lung Injury

Khazdair

Bargi

Saadat

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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“…Reactive oxygen species (ROS) play a pivotal role in inflammation ( 16 ). Under normal condition, ROS are neutralized by antioxidants so as to maintain the balance of the oxidant and antioxidant system; under pathologic conditions, the level of ROS is expected to be increased and the activity of the antioxidant system decreased, directly leading to an imbalance trending to oxidation, termed oxidative stress ( 17 , 18 ). As oxidative stress is an important process during the pathophysiology of inflammatory diseases, including pulmonary inflammation ( 19 ), the present study examined the levels of ROS and antioxidant-oxidant enzymes including MDA, LDH and SOD to verify the effect of UCF-101 on oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of HtrA2 alleviates inflammatory response and cell apoptosis in lipopolysaccharide‑induced acute pneumonia in rats

Wang

2020

Mol Med Rep

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Pneumonia is one of the commonest causes of death worldwide. High-temperature requirement a2 (Htra2) is a proapoptotic mitochondrial serine protease involved in caspase-dependent or caspase-independent cell apoptosis. ucF-101 (5-[5-(2-nitrophenyl) furfuryl iodine]-1,3-diphenyl-2-thiobarbituric acid), an inhibitor of Htra2, has a protective effect on organs in various diseases by inhibiting cell apoptosis. The aim of the present study was to explore whether ucF-101 has a protective effect on lungs in pneumonia. a lipopolysaccharide (lPS)-induced pneumonia model was established in rats. ucF-101 (2 µmol/kg) was used for treatment. lung injury was detected by hematoxylin and eosin staining. Pro-inflammatory cytokines and oxidative stress-related factors were detected using corresponding test kits. Tunel staining was used to measure the amount of cell apoptosis. apoptosis-associated proteins were detected by western blot assay. The present study indicated pulmonary injury induced by lPS. Treatment with ucF-101 clearly alleviated this pulmonary damage and restored the levels of pro-inflammatory cytokines and oxidative stress-related factors. in addition, ucF-101 significantly reduced lPS-induced cell apoptosis, the release of Htra2 and cytochrome from mitochondria to the cytoplasm and inhibited the expression of pro-apoptotic proteins. ucF-101 also restored the aTP level. The present results demonstrated that ucF-101 acts as a positive regulator of acute pneumonia by inhibiting inflammatory response, oxidative stress and mitochondrial apoptosis. The present study suggests ucF-101 as a potential candidate for pneumonia therapy.

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Epithelial Dysfunction in Lung Diseases: Effects of Amino Acids and Potential Mechanisms

Chen

Jin

Yang

et al. 2020

Advances in Experimental Medicine and Biology

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Lung diseases affect millions of individuals all over the world. Various environmental factors, such as toxins, chemical pollutants, detergents, viruses, bacteria, microbial dysbiosis, and allergens, contribute to the development of respiratory disorders. Exposure to these factors activates stress responses in host cells and disrupt lung homeostasis, therefore leading to dysfunctional epithelial barriers. Despite significant advances in therapeutic treatments for lung diseases in the last two decades, novel interventional targets are imperative, considering the side effects and limited efficacy in patients treated with currently available drugs. Nutrients, such as amino acids (e.g., arginine, glutamine, glycine, proline, taurine, and tryptophan), peptides, and bioactive molecules, have attracted more and more attention due to their abilities to reduce oxidative stress, inhibit apoptosis, and regulate immune responses, thereby improving epithelial barriers. In this review, we summarize recent advances in amino acid metabolism in the lungs, as well as multifaceted functions of amino acids in attenuating inflammatory lung diseases based on data from studies with both human patients and animal models. The underlying mechanisms for the effects of physiological amino acids are likely complex and involve cell signaling, gene expression, and anti-oxidative reactions. The beneficial effects of amino acids are expected to improve the respiratory health and well-being of humans and other animals. Because viruses (e.g., coronavirus) and environmental pollutants (e.g., PM2.5 particles) induce severe damage to the lungs, it is important to determine whether dietary supplementation or intravenous administration of individual functional amino acids (e.g., arginine-HCl, citrulline, N-acetylcysteine, glutamine, glycine, proline and tryptophan) or their combinations to affected subjects may alleviate injury and dysfunction in this vital organ.

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The effect of captopril on lipopolysaccharide-induced lung inflammation

Cited by 18 publications

References 37 publications

Thymoquinone Ameliorates Lung Inflammation and Pathological Changes Observed in Lipopolysaccharide-Induced Lung Injury

Thymoquinone Ameliorates Lung Inflammation and Pathological Changes Observed in Lipopolysaccharide-Induced Lung Injury

Inhibition of HtrA2 alleviates inflammatory response and cell apoptosis in lipopolysaccharide‑induced acute pneumonia in rats

Epithelial Dysfunction in Lung Diseases: Effects of Amino Acids and Potential Mechanisms

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