Effects of cannabinoid receptor 2 synthetic agonist, AM1241, on bleomycin induced pulmonary fibrosis

Parlar, Ali İhsan; Arslan, Seyfullah Oktay; Yumrutaş, Önder; Elibol, Ebru; Yalcin, Alper; Üçkardeş, Fatih; Aydın, Hasan Emre; Doğan, Muhammed Fatih; Kuştepe, Elif Kayhan; Özer, Mehmet Kaya

doi:10.1080/10520295.2020.1758343

Cited by 11 publications

(3 citation statements)

References 29 publications

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“…In this study bleomycin produced loss of normal lung architectures with many collapsed alveoli, marked inflammatory cell infiltration, marked thickened alveolar septa and partial obliterated bronchiole and significant increase in main area percent of collagen fibers deposition and caspase-3immuno-positive expression in comparison with that in group I. This result is in agreement with a previous histopathological study which detected loss of lung architecture in most of lung sections from bleomycin group, and replacement of the lung tissue with fibrous tissue (22) .Similarly Parlar et al added that bleomycin induced areas of necrosis and inflammation in lung sections with increased the accumulation of collagen fibers and extracellular matrix especially peribronchial (23) . In the same line, Alia, et al (21) found that the histopathological study of bleomycin group showed a significant increase in fibrosis score, adding together to, a significant increase in H-score of fibrosis of α-SMA immunehistochemical stain compared to the control group.…”

Section: Discussionsupporting

confidence: 90%

The Possible Protective Effect of Melatonin and Coenzyme Q10 on Lung Injury Induced by Bleomycin in Adult Male Albino Rats

Elkerdasy

Elshazly

Baioumy

et al. 2021

The Egyptian Journal of Hospital Medicine

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Background: bleomycin-induced lung toxicity and oxidative damage by decreasing the deactivating enzyme, genetic vulnerability, and released cytokines of inflammation. Melatonin has a free radical detoxifying effect, coenzyme Q10 has a strong antioxidant effect. Aim of the study: this study aimed to evaluate the possible protective role of melatonin and coenzyme Q10 in bleomycin-induced lung injury in Albino rats. Material and Methods: forty male Albino rats were categorized into five groups; group I (control group), group II (bleomycin group): rats were given a single dose of bleomycin intra-tracheal for inducing lung injury, group III (melatonin group): rats were given melatonin for three weeks after intratracheal installation of bleomycin, group IV (coenzymeQ10 group): rats were given coenzymeQ10 for three weeks after intratracheal installation of bleomycin and group V (combined melatonin and Co Q10 group): rats were given a combination of melatonin and coenzyme Q10for three weeks after induction of bleomycin lung toxicity. Lung tissues were prepared for biochemical, histological and immunohistochemical studies. Results: bleomycin produced a significant increase in the level of malondialdehyde and a significant reduction in glutathione peroxidase activity in lung tissues with loss of normal histological lung architecture, significant elevation in main area percent of collagen fibers deposition and caspase-3 immuno positive expression. In group III melatonin enhanced a significant improvement in the biochemical changes, moderate prevention of histopathological changes in lung tissue with a significant reduction in main area percent of collagen fibers deposition and caspase-3 immuno positive expression. While, in group IV co enzyme Q10 enhanced non significant improvement in the biochemical changes, mild prevention of histopathological changes and non-significant reduction in main area percent of collagen fibers deposition and caspase-3 immuno positive expression. Using a combination of both drugs in group V enhanced a significant improvement in the biochemical changes and almost preservation of normal histological architecture of the lung tissue. Conclusion: administration of both melatonin and coenzyme Q10 produced almost a complete recovery of bleomycin induced lung injury.

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Section: Discussionsupporting

confidence: 90%

The Possible Protective Effect of Melatonin and Coenzyme Q10 on Lung Injury Induced by Bleomycin in Adult Male Albino Rats

Elkerdasy

Elshazly

Baioumy

et al. 2021

The Egyptian Journal of Hospital Medicine

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“…Treatment with the CB 2 receptor agonist BCP prevents glutathione depletion, enhances antioxidant enzyme activity in the midbrain, and inhibits the elevation of nitrite levels. It has been found that the GW405833 (a CB 2 receptorspecific agonist) administration inhibits inflammatory response by suppressing the levels of cytokine and oxidative stress (Parlar et al, 2018). Other research results report that the CB 2 receptor agonist HU308 reduces the production of ROS-generating enzymes NOX4, NOX2, and NOX1, as well as subsequent renal oxidative stress in mice (Zhang et al, 2009).…”

Section: The Inhibitory Effect Of Cb 2 Receptor On Oxidative Stressmentioning

confidence: 97%

Research progress on the cannabinoid type-2 receptor and Parkinson’s disease

Yu,

Jia,

Dong

2024

Front. Aging Neurosci.

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Parkinson’s disease (PD) is featured by movement impairments, including tremors, bradykinesia, muscle stiffness, and imbalance. PD is also associated with many non-motor symptoms, such as cognitive impairments, dementia, and mental disorders. Previous studies identify the associations between PD progression and factors such as α-synuclein aggregation, mitochondrial dysfunction, inflammation, and cell death. The cannabinoid type-2 receptor (CB2 receptor) is a transmembrane G-protein-coupled receptor and has been extensively studied as part of the endocannabinoid system. CB2 receptor is recently emerged as a promising target for anti-inflammatory treatment for neurodegenerative diseases. It is reported to modulate mitochondrial function, oxidative stress, iron transport, and neuroinflammation that contribute to neuronal cell death. Additionally, CB2 receptor possesses the potential to provide feedback on electrophysiological processes, offering new possibilities for PD treatment. This review summarized the mechanisms underlying PD pathogenesis. We also discussed the potential regulatory role played by CB2 receptor in PD.

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“…Moreover, Δ 9 -tetrahydrocannabinolic acid (Δ 9 -THCA), the non-psychotropic precursor of Δ 9 -THC can also prevent TGF-β-induced liver fibrosis [ 112 ]. Although the effects of cannabinoids on lung fibrosis are not clear, a recent study showed that activation of cannabinoid receptor 2 (CB2) protects against bleomycin-induced fibrosis [ 113 ].…”

Section: Modulation Of Pulmonary Ace2 Expressionmentioning

confidence: 99%

Involvement of the ACE2/Ang-(1–7)/MasR Axis in Pulmonary Fibrosis: Implications for COVID-19

Morganstein

Haidar

Trivlidis

et al. 2021

IJMS

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Pulmonary fibrosis is a chronic, fibrotic lung disease affecting 3 million people worldwide. The ACE2/Ang-(1–7)/MasR axis is of interest in pulmonary fibrosis due to evidence of its anti-fibrotic action. Current scientific evidence supports that inhibition of ACE2 causes enhanced fibrosis. ACE2 is also the primary receptor that facilitates the entry of SARS-CoV-2, the virus responsible for the current COVID-19 pandemic. COVID-19 is associated with a myriad of symptoms ranging from asymptomatic to severe pneumonia and acute respiratory distress syndrome (ARDS) leading to respiratory failure, mechanical ventilation, and often death. One of the potential complications in people who recover from COVID-19 is pulmonary fibrosis. Cigarette smoking is a risk factor for fibrotic lung diseases, including the idiopathic form of this disease (idiopathic pulmonary fibrosis), which has a prevalence of 41% to 83%. Cigarette smoke increases the expression of pulmonary ACE2 and is thought to alter susceptibility to COVID-19. Cannabis is another popular combustible product that shares some similarities with cigarette smoke, however, cannabis contains cannabinoids that may reduce inflammation and/or ACE2 levels. The role of cannabis smoke in the pathogenesis of pulmonary fibrosis remains unknown. This review aimed to characterize the ACE2-Ang-(1–7)-MasR Axis in the context of pulmonary fibrosis with an emphasis on risk factors, including the SARS-CoV-2 virus and exposure to environmental toxicants. In the context of the pandemic, there is a dire need for an understanding of pulmonary fibrotic events. More research is needed to understand the interplay between ACE2, pulmonary fibrosis, and susceptibility to coronavirus infection.

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Effects of cannabinoid receptor 2 synthetic agonist, AM1241, on bleomycin induced pulmonary fibrosis

Cited by 11 publications

References 29 publications

The Possible Protective Effect of Melatonin and Coenzyme Q10 on Lung Injury Induced by Bleomycin in Adult Male Albino Rats

The Possible Protective Effect of Melatonin and Coenzyme Q10 on Lung Injury Induced by Bleomycin in Adult Male Albino Rats

Research progress on the cannabinoid type-2 receptor and Parkinson’s disease

Involvement of the ACE2/Ang-(1–7)/MasR Axis in Pulmonary Fibrosis: Implications for COVID-19

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