Therapeutic effects of minocycline on oleic acid-induced acute respiratory distress syndrome (ARDS) in rats

Abstract

Acute respiratory distress syndrome (ARDS) is a serious intensive care condition. Despite advances in treatment over the previous few decades, ARDS patients still have high fatality rates. Thus, more research is needed to improve the outcomes for people with ARDS. Minocycline is an antibiotic with antioxidant, anti-inflammatory, and anti-apoptotic effects. In the current investigation, the therapeutic effects of minocycline on oleic acid-induced ARDS were evaluated. Male rats were classified into 6 groups, 1. control (normal saline), 2. oleic acid (100 µL, i.v.), 3–5. oleic acid + minocycline (50, 100, 200 mg/kg, i.p.), and 6. minocycline (200 mg/kg, i.p.) alone. Twenty-four hours after the oleic acid injection, the lung tissue is isolated, weighed, and the middle part of the right lung is immediately placed in the freezer, while the middle part of the left lung is placed in formalin and sent to the laboratory for pathology testing. Then, the amounts of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), cytokines (interleukin-1 beta (IL-1β), tumor necrosis factor-α (TNF-α)), B-cell lymphoma 2 (Bcl-2), Bcl-2 associated X (Bax), and cleaved caspase-3 were determined in lung tissue. Administration of oleic acid increased emphysema, inflammation, vascular congestion, hemorrhage, MDA amount, Bax/Bcl-2 ratio, cleaved caspase-3, IL-1β, TNF-α levels, and decreased GSH, SOD, and CAT levels in comparison with the control group. The administration of minocycline could significantly reduce pathological and biochemical alterations induced by oleic acid. Minocycline has a therapeutic effect on oleic acid-induced ARDS through antioxidant, anti-inflammatory, and anti-apoptotic properties. Graphical abstract

Mechanism and Experimental Verification of Rhodiola rosea L. for the Treatment of Acute Lung Injury Through Network Pharmacology and Molecular Docking

“…ALI delineates the acute hypoxic respiratory insufficiency or respiratory failure stemming from diffuse pulmonary interstitial and alveolar edema, induced by the injury to pulmonary capillary endothelial cells and alveolar epithelial cells in noncardiac diseases such as severe infection, shock, trauma, and burns. The progression to ARDS 20–22 is feasible when the inflicted injury reaches a critical threshold. Notably, a specific pharmacological intervention for treating ALI remains elusive, and prevailing therapeutics in clinical practice exhibit drawbacks, encompassing proclivity for adverse reactions such as coagulation disorders, gastric ulcers, and osteoporosis.…”