Respiratory system — efficacy & protocols
Professional nebulized exosome solutions for respiratory mucosal repair and pulmonary anti-inflammation, with clear onset timelines and the underlying targeting principle.
A professional-grade R&D solution designed for respiratory mucosal repair and pulmonary anti-inflammation. It combines advanced nebulization technology with the bioactivity of high-purity exosomes to act directly on microscopic lesions — a professional-quality choice for respiratory symptoms and mucosal-damage repair.
- Nano-Targeting: Nebulization delivers nanoparticles directly to microscopic lesions in the airways and distal alveoli — fast-acting, high local concentration, safe and convenient — an innovative non-invasive delivery approach.
- Barrier Remodelling: At the molecular level, by down-regulating inflammatory expression such as IL-6 and TNF-α, it blocks the inflammatory cascade and induces the body’s own repair and regeneration.
- Highest Standards: Strictly following 533-point full-process quality control — sterility, endotoxin, mycoplasma and virus all screened; no hormones, no antibiotics, no dilators — ensuring absolute safety for mucosal contact with no dependence.
Airway Anti-inflammatory Repair
Reduce airway inflammation, ease cough, chest tightness and shortness of breath.
cough and chest tightness reduced, breathing becomes easier
inflammation is relieved, sputum reduced
airway barrier is repaired, probability of recurrent infection is reduced
How to use: Prioritize Nebulized Inhalation; Avoid irritants such as smoke, alcohol, dust, and cold air.
Targeting principle & mechanism
Core functional proteins: IL-10, IL-1Ra, sTNFR, TGF-β3, HSP70, SOD, KGF, lactoferrin, IDO
Targets: Airway ciliated epithelium, submucosal macrophages, airway smooth muscle, bronchial T cells
Targeting logic: Asthma, COPD and infection-driven airway inflammation secretes high CXCL12 and exposes integrin receptors on damaged epithelium; the exosome’s CXCR4 reads the inflammation gradient and anchors only to swollen, damaged airway mucosa, sparing healthy bronchial epithelium.
- IL-1Ra and sTNFR neutralise airway TNF-α and IL-6, blocking the NF-κB cascade to quickly reduce swelling, mucus over-secretion and bronchospasm.
- IL-10 and TGF-β3 reprogram M1 macrophages to reparative M2 and balance Th1/Th2 immunity, lowering airway hyper-reactivity, cough and wheeze.
- HSP70 and SOD clear oxidative free radicals, easing epithelial damage from smoke, viruses and pollutants.
- KGF repairs ciliated epithelium and restores the mucosal barrier, reducing entry of particles and pathogens.
- Lactoferrin suppresses harmful colonisation and IDO induces regulatory T cells, preventing chronic recurrent inflammation and airway-remodelling fibrosis.
Alveolar Damage Repair
Regenerate alveolar and pulmonary microvascular cells, repair air-blood barrier and recover lung function.
dyspnea on exertion improved, lung function indicators increased
damaged alveoli are gradually repaired, blood oxygen status improved
lung tissue is remodeled, exercise endurance enhanced
How to use: Use Via Nebulizer; avoid strenuous exercise during the recovery period, prioritize gentle aerobic exercise.
Targeting principle & mechanism
Core functional proteins: KGF, EGF, bFGF, VEGF, BMPR2, TGF-β3, fibronectin, MMP inhibitors, SOD, IL-10, ENaC regulators
Targets: Type II (AT2) & type I (AT1) alveolar cells, alveolar macrophages, alveolar capillary endothelium, interstitial fibroblasts
Targeting logic: Pneumonia, acute lung injury and fibrosis break alveolar septa and cause collapse and oedema, releasing high CXCL12; exosomes pass through the airway into the alveolar space and bind damaged AT2 stem cells and broken microvascular endothelium.
- KGF and EGF activate AT2 stem-cell proliferation and drive AT2→AT1 differentiation via BMPR2–SMAD to rebuild the gas-exchange structure and repair the alveolar wall.
- VEGF regenerates alveolar microvasculature and repairs the endothelial barrier, reducing exudation and oedema; ENaC speeds clearance of intra-alveolar fluid.
- TGF-β3 + MMP inhibitors restrain over-activated fibroblasts and block abnormal collagen build-up, preventing alveolar fibrosis and stiffening.
- Fibronectin rebuilds the alveolar matrix scaffold and repairs broken septa, preventing alveolar fusion and collapse.
- IL-10 and SOD suppress local inflammation and oxidative stress, reducing epithelial apoptosis and maintaining stable ventilation.
Pulmonary Anti-fibrosis
Inhibit excessive fibroblast proliferation and collagen deposition, relieve pulmonary fibrosis.
dry cough and wheezing reduced, lesions on imaging become lighter
fibrotic tissue is gradually improved, lung elasticity restored
disease progression is significantly slowed down, ventilation function restored
How to use: Use regularly and consistently without interruption; strictly abstain from smoking and stay away from smog and dust.
Targeting principle & mechanism
Core functional proteins: TGF-β3, HGF, BMP-7, MMP inhibitors, IL-10, HSP70, SOD, decorin, FGF inhibitors, PDGF antagonists
Targets: Interstitial fibroblasts, myofibroblasts, alveolar epithelium, pulmonary vascular smooth muscle, alveolar macrophages
Targeting logic: In fibrotic lesions, fibroblasts are over-activated with abnormal collagen, continuously releasing pro-fibrotic signals (CXCL12, TGF-β1); exosomes home via CXCR4 to the lesion and target activated fibroblasts, sparing normal parenchyma.
- TGF-β3 and decorin competitively block the pro-fibrotic TGF-β1/Smad pathway, inhibiting fibroblast-to-myofibroblast conversion and cutting abnormal collagen at the source.
- HGF and BMP-7 regenerate alveolar epithelium, repair damaged walls and reverse epithelial–mesenchymal transition (EMT), reducing lesion formation.
- MMP inhibitors rebalance metalloproteinases and their inhibitors, degrading deposited abnormal collagen and easing stiffness.
- PDGF antagonists inhibit pulmonary vascular smooth-muscle proliferation, reducing vascular remodelling and improving circulation.
- IL-10, HSP70 and SOD suppress chronic inflammation and oxidative stress, lowering fibrosis drivers and slowing functional decline.
How exosomes target the respiratory tract
Core functional proteins: CD9 / CD63 / CD81 tetraspanins, integrins, ICAM adhesion proteins, chemokine receptor CXCR4
Targets: Damaged airway and alveolar mucosa and their target cells
- Targeted recognition: the exosome membrane carries a molecular “postal code” that binds matching ligands on damaged airway / alveolar cells, actively grabbing the lesion while barely retaining on healthy tissue.
- Inhaled (non-invasive) delivery: nebulized 30–150 nm particles reach the airways and distal alveoli; with their phospholipid bilayer they enter cells intact via both passive penetration and active endocytosis, without being broken down.
- Intracellular release: once inside the cell the membrane fuses and ruptures, releasing functional proteins that directly regulate cell genes and signalling pathways — calming inflammation and repairing the mucosa from the root.