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Treatment of Sulfur Dioxide-Induced Lung Injury in Rats
PDPI Jatim, 07 Ags 2019 18:36:37


Inhalation of sulfur dioxide (SO2) primarily affects the lungs and exposure to high concentrations can be immediately dangerous to life. The response after inhalation of SO2 implicates that the early response involves tissue injury, neutrophilic lung inflammation and airway hyperresponsiveness (AHR). In rats, lung fibrosis is evident 14 days post exposure and early treatment with a single dose of Dexamethasone (DEX) significantly down-modulates the acute inflammatory response in airways. However, this treatment is not sufficient for complete protection against the pulmonary toxicity.

The aim was to evaluate whether repeated treatment with DEX alone or in combination with the antioxidant N-acetyl-L-cysteine(NAC) and the anti-fibrotic substance, Pirfenidone (PFD), administered 1h, 5h and 23h after SO2-exposure (2200ppm, 10min) could counteract the inflammatory responses, AHR and lung fibrosis in Sprague-Dawley rats.

All treatment approaches significantly reduced the total leukocyte response but only combined DEX and NAC reduced the number of neutrophils in BAL. PFD reduced methacholine-induced AHR to almost control levels, in contrast to DEX and DEX/NAC which only provided partial protection against AHR. Only DEX treatment reduced the collagen formation in lung tissue.

In conclusion, all treatment protocols reduced the acute SO2-induced inflammatory response in airways with DEX/NAC treatment slightly more efficient than the other protocols. PFD appeared to be more efficient than DEX and DEX/NAC combination in reduction of AHR. Only DEX treatment was efficient in the reduction of long-term effects monitored 14 days post exposure. In the future, studies addressing both anti-inflammatory and anti-fibrotic treatment is higly motivated.

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