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<p>Comorbid depression is greatly predominant among COPD patients. Nevertheless, comorbid depression associated with COPD is frequently unidentified, and pathogenic exploration is too inadequate. Exposure to cigarette smoke (CS) contributes to inflammation and oxidative stress (OS), which are basic components in the pathogenesis of lung disorders of COPD. Robinin (RB), a kaempferol derivative of flavonoid glycoside, possesses neuroprotective, antioxidative, and anti-inflammatory properties. Hence, our research has evaluated the neuroprotective effect of RB on the CS-induced COPD mouse model. C57BL/6J mice were randomly assigned to 5 groups, each comprising 6 mice. Normal control (NC), CS, CS + RB (25&#xa0;mg/kg bw), CS + RB (50&#xa0;mg/kg bw), and CS + Dexamethasone (DEX, 5&#xa0;mg/kg bw). CS was exposed to the COPD development to assess the mice’s body weight, neurological dysfunction, depression-interrelated behaviours, blood cellularity, oxidative stress, neuroinflammation, cytokines, immune cells, neurotransmitters, inflammatory signalling cascade, and histopathology of lungs, as well as the hippocampus. RB could attenuate body weight loss, oxidative stress, neuroinflammation, neurological impairments, immune cell infiltration, cytokine levels, and histopathological alterations, as well as immunohistochemistry, in a concentration-dependent manner by enhancing neurotransmitter levels. Our findings established that the neuroprotective and anti-inflammatory activities of RB against CS-exposed COPD with comorbid depression are achieved by suppressing PI3K/AKT-mediated NF-κB/NLRP3 signalling pathways.</p>

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Robinin alleviates oxidative stress and inflammation in cigarette smoke exposed COPD-induced depression via inhibiting P13K/AKT-mediated NF-κB/NLRP3 signalling pathway

  • 期刊论文

  • 发表日期：

    2026年6月15日

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  • Yin Junhai,
  • Liu Bao

摘要

Comorbid depression is greatly predominant among COPD patients. Nevertheless, comorbid depression associated with COPD is frequently unidentified, and pathogenic exploration is too inadequate. Exposure to cigarette smoke (CS) contributes to inflammation and oxidative stress (OS), which are basic components in the pathogenesis of lung disorders of COPD. Robinin (RB), a kaempferol derivative of flavonoid glycoside, possesses neuroprotective, antioxidative, and anti-inflammatory properties. Hence, our research has evaluated the neuroprotective effect of RB on the CS-induced COPD mouse model. C57BL/6J mice were randomly assigned to 5 groups, each comprising 6 mice. Normal control (NC), CS, CS + RB (25 mg/kg bw), CS + RB (50 mg/kg bw), and CS + Dexamethasone (DEX, 5 mg/kg bw). CS was exposed to the COPD development to assess the mice’s body weight, neurological dysfunction, depression-interrelated behaviours, blood cellularity, oxidative stress, neuroinflammation, cytokines, immune cells, neurotransmitters, inflammatory signalling cascade, and histopathology of lungs, as well as the hippocampus. RB could attenuate body weight loss, oxidative stress, neuroinflammation, neurological impairments, immune cell infiltration, cytokine levels, and histopathological alterations, as well as immunohistochemistry, in a concentration-dependent manner by enhancing neurotransmitter levels. Our findings established that the neuroprotective and anti-inflammatory activities of RB against CS-exposed COPD with comorbid depression are achieved by suppressing PI3K/AKT-mediated NF-κB/NLRP3 signalling pathways.