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Table 2 Relevant studies focusing on liposomes for oxidative stress

From: Novel drug delivery systems targeting oxidative stress in chronic obstructive pulmonary disease: a review

Nanocarrier composition

Drug

Method of preparation

Size

Route of administration

Mode of action

Ref

DPPC, cholesterol and stearylamine

CAT or SOD

Reverse-phase evaporation

–

Intravenous

Decrease lipid peroxidation products (malondialdehyde, conjugated dienes, lipid hydroperoxides)

[93]

DPPC

a-Tocopherol

Reverse-phase evaporation

320 ± 40 nm

Intratracheal

Reduce myeloperoxidase activity and reverse of phorbol myristate acetate-induced changes in lung edema, lipid peroxidation, enzyme and alkaline phosphatase activities

[94]

DPPC and cholesterol

Cu, Zn SOD and CAT

Reverse-phase evaporation

200 nm

Intratracheal, instillation

Increase antioxidant activity of alveolar type II cell, increase lung antioxidant enzyme levels

[95, 96]

DPPC

SOD and/or CAT

Reverse-phase evaporation

0.1–0.4 Î¼m

Intratracheal

Prevent the chronic vascular and parenchymal damage due to oxygen toxicity

[97]

DPPC

NAC

Reverse-phase evaporation

-

Intratracheal

Increase pulmonary glutathione

[98]

DPPC

NAC, glutathione, a-tocopherol

Thin-film hydration method

100 nm

Intratracheal instillation

Reduce CINC-1, IL-1β, and TNF-α

[99]

Phospholipid and cholesterol

NAC

Reverse phase evaporation and spray drying

∼100 nm

Inhalation

Against TBARS production

[100]

DPPC

a-Tocopherol

Solvent evaporation method

-

Intraperitoneal, injection

Reduce acute inflammatory, cell influx and suppress collagen formation in lung tissue

[101]

Chitosan, hyaluronan, and phospholipids

Curcumin

Sonication, stirring

130 nm

A549 cells

Cell relative metabolic activity ≥ 80% after treated with hydrogen peroxide

[102]

  1. DPPC: L-a-dipalmitoylphosphatidyl-choline; NAC: N-acetylcysteine; TBARS: thiobarbituric acid reactive species