Cannabidiol May Treat Inflammatory Lung Diseases, According to New Study

Cannabidiol has a strong anti-inflammatory effect, and can also improve lung function in those with acutelung lung injury, indicating that it may be a viable treatment option for inflammatory lung diseases, according to a new study published in the journal Immunopharmacology Immunotoxicology.

According to the study; “We have previously shown that the prophylactic treatment with cannabidiol (CBD) reduces inflammation in a model of acute lung injury (ALI). In this work we analyzed the effects of the therapeutic treatment with CBD in mice subjected to the model of lipopolysaccharide (LPS)-induced ALI on pulmonary mechanics and inflammation.”

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Cannabinoid Receptor Activation May Protect Against Acute Lung Injury

A study published recently by the Journal BioMed Research International has found that cannabinoid receptor activationlung may protect against acute lung injury caused by the herbicide Paraquat.

According to researchers at the Department of Emergency Medicine at Shengjing Hospital of China Medical University; “Paraquat, a widely used herbicide, is well known to exhibit oxidative stress and lung injury. In the present study, we investigated the possible underlying mechanisms of cannabinoid receptor-2 (CB2) activation to ameliorate the proinflammatory activity induced by PQ [Paraquat] in rats.”

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Cannabinoids Can Treat Acute Lung Injury, According to New Study

A new study published in the journal PLOS One as well as the National Institute of Health has found that cannabinoids can be an effective treatment for acute lung injury, or acute respiratory distress syndrome (ARDS)bud, which is a condition caused by damage or disease to the lungs, which is often life-threatening.

The study, which was conducted by researchers at the University of São Paulo, found that: “MAGL inhibition, and consequently the increase in 2-AG levels [a naturally-occurring cannabinoid], produced anti-inflammatory effects in a murine model of LPS-induced ALI, a finding that was considered a consequence of the activation of the CB1 and CB2 receptors.”

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