Effects of Mikania glomerata Spreng. and Mikania laevigata Schultz Bip. ex Baker (Asteraceae) extracts on pulmonary inflammation and oxidative stress caused by acute coal dust exposure.
Several studies have reported biological effects of Mikania glomerata and Mikania laevigata, used in Brazilian folk medicine for respiratory diseases. Pneumoconiosis is characterized by pulmonary inflammation caused by coal dust exposure. In this work, we evaluated the effect of pretreatment with M. glomerata and M. laevigata extracts (MGE and MLE, respectively) (100 mg/kg, s.c.) on inflammatory and oxidative stress parameters in lung of rats subjected to a single coal dust intratracheal instillation. Rats were pretreated for 2 weeks with saline solution, MGE, or MLE. On day 15, the animals were anesthetized, and gross mineral coal dust or saline solutions were administered directly in the lung by intratracheal instillation. Fifteen days after coal dust instillation, the animals were killed. Bronchoalveolar lavage (BAL) was obtained; total cell count and lactate dehydrogenase (LDH) activity were determined. In the lung, myeloperoxidase activity, thiobarbituric acid-reactive substances (TBARS) level, and protein carbonyl and sulfhydryl contents were evaluated. In BAL of treated animals, we verified an increased total cell count and LDH activity. MGE and MLE prevented the increase in cell count, but only MLE prevented the increase in LDH. Myeloperoxidase and TBARS levels were not affected, protein carbonylation was increased, and the protein thiol levels were decreased by acute coal dust intratracheal administration. The findings also suggest that both extracts present an important protective effect on the oxidation of thiol groups. Moreover, pretreatment with MGE and MLE also diminished lung inflammatory infiltration induced by coal dust, as assessed by histopathologic analyses. The present study indicates that M. glomerata and M. laevigata might become good candidates for the prevention of lung oxidative injury caused by coal dust exposure.
Freitas
Tiago P
TP
Laboratório de Fisiopatologia Experimental, Universidade do Extremo Sul Catarinense, Criciúma, Santa Catarina, Brazil.
Silveira
Paulo C
PC
Rocha
Luís G
LG
Rezin
Gislaine T
GT
Rocha
João
J
Citadini-Zanette
Vanilde
V
Romão
Pedro T
PT
Dal-Pizzol
Felipe
F
Pinho
Ricardo A
RA
Andrade
Vanessa M
VM
Streck
Emilio L
EL
D000393:Air Pollutants / Q000009:adverse effects; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D018893:Bronchoalveolar Lavage; D002452:Cell Count; D016923:Cell Death; D003031:Coal / Q000009:adverse effects*; D004391:Dust; D004781:Environmental Exposure / Q000009:adverse effects; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D055370:Lung Injury / Q000517:prevention & control*; D008297:Male; D035742:Mikania; D018384:Oxidative Stress / Q000187:drug effects*; D009195:Peroxidase / Q000378:metabolism; D008517:Phytotherapy; D018515:Plant Leaves; D011014:Pneumonia / Q000517:prevention & control*; D050050:Protein Carbonylation; D051381:Rats; D017208:Rats, Wistar; D013438:Sulfhydryl Compounds / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
D000393:Air Pollutants; D000975:Antioxidants; D003031:Coal; D004391:Dust; D013438:Sulfhydryl Compounds; D017392:Thiobarbituric Acid Reactive Substances; D007770:L-Lactate Dehydrogenase; D009195:Peroxidase