关键词: C-phycocyanin airway remodeling asthma inflammation ovalbumin

Mesh : Animals Phycocyanin / pharmacology therapeutic use Asthma / drug therapy metabolism chemically induced Oxidative Stress / drug effects Ovalbumin / adverse effects Rats Airway Remodeling / drug effects Rats, Sprague-Dawley Disease Models, Animal Inflammation / metabolism drug therapy Male Lung / drug effects pathology metabolism Cytokines / metabolism

来  源:   DOI:10.3390/ijms25137031   PDF(Pubmed)

Abstract:
Asthma is a chronic immunological disease related to oxidative stress and chronic inflammation; both processes promote airway remodeling with collagen deposition and matrix thickening, causing pulmonary damage and lost function. This study investigates the immunomodulation of C-phycocyanin (CPC), a natural blue pigment purified from cyanobacteria, as a potential alternative treatment to prevent the remodeling process against asthma. We conducted experiments using ovalbumin (OVA) to induce asthma in Sprague Dawley rats. Animals were divided into five groups: (1) sham + vehicle, (2) sham + CPC, (3) asthma + vehicle, (4) asthma + CPC, and (5) asthma + methylprednisolone (MP). Our findings reveal that asthma promotes hypoxemia, leukocytosis, and pulmonary myeloperoxidase (MPO) activity by increasing lipid peroxidation, reactive oxygen and nitrogen species, inflammation associated with Th2 response, and airway remodeling in the lungs. CPC and MP treatment partially prevented these physiological processes with similar action on the biomarkers evaluated. In conclusion, CPC treatment enhanced the antioxidant defense system, thereby preventing oxidative stress and reducing airway inflammation by regulating pro-inflammatory and anti-inflammatory cytokines, consequently avoiding asthma-induced airway remodeling.
摘要:
哮喘是一种与氧化应激和慢性炎症相关的慢性免疫性疾病,两者均促进气道重塑,胶原沉积和基质增厚,导致肺损伤和功能丧失。这项研究调查了C-藻蓝蛋白(CPC)的免疫调节,从蓝藻中纯化的天然蓝色色素,作为预防哮喘重塑过程的潜在替代疗法。我们使用卵清蛋白(OVA)在SpragueDawley大鼠中进行了诱导哮喘的实验。动物分为五组:(1)假手术+载体,(2)假+CPC,(3)哮喘+车辆,(4)哮喘+CPC,(5)哮喘+甲基强的松龙(MP)。我们的发现表明哮喘会促进低氧血症,白细胞增多,和肺髓过氧化物酶(MPO)活性通过增加脂质过氧化,活性氧和氮,与Th2反应相关的炎症,和肺部的气道重塑。CPC和MP治疗部分阻止了这些生理过程,对所评估的生物标志物具有类似的作用。总之,CPC治疗增强了抗氧化防御系统,从而通过调节促炎和抗炎细胞因子来预防氧化应激和减少气道炎症,因此避免哮喘诱导的气道重塑。
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