Propolis reverses acetaminophen induced acute hepatorenal alterations: a biochemical and histopathological approach.
The present study has been conducted to evaluate the curative effect of propolis extract, a honey bee-hive product, against acetaminophen (APAP) induced oxidative stress and dysfunction in liver and kidney. Animals were challenged with APAP (2 g/kg, p.o.) followed by treatment of propolis extract (100 and 200 mg/kg, p.o.) once only after 24 h. Release of transaminases, alkaline phosphatase, lactate dehydrogenase, and serum bilirubin were increased, whereas hemoglobin and blood sugar were decreased after APAP administration. Antioxidant status in both the liver and kidney tissues were estimated by determining the glutathione, malondialdehyde content and activities of the CYP enzymes, which showed significant alterations after APAP intoxication. In addition, activities of adenosine triphosphatase, acid phosphatase, alkaline phosphatase, and major cell contents (total protein, glycogen and cholesterol) were also altered due to APAP poisoning. Propolis extract successfully reversed the alterations of these biochemical variables at higher dose. Improvements in hepatorenal histoarchitecture were also consistent with biochemical observations. The results indicated that ethanolic extract of propolis has ability to reverse APAP-induced hepatorenal biochemical and histopathological alterations probably by increasing the antioxidative defense activities due to various phenolic compounds present in it.
Nirala
Satendra Kumar
SK
Reproductive Biology and Toxicology Laboratory, School of Studies in Zoology, Jiwaji University, Gwalior (M.P.), India.
Bhadauria
Monika
M
D000082:Acetaminophen; D000135:Acid Phosphatase / Q000378:metabolism; D000251:Adenosine Triphosphatases / Q000378:metabolism; D000469:Alkaline Phosphatase / Q000097:blood; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001663:Bilirubin / Q000097:blood; D001786:Blood Glucose / Q000187:drug effects; D056486:Chemical and Drug Induced Liver Injury; D002784:Cholesterol / Q000378:metabolism; D003577:Cytochrome P-450 Enzyme System / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005260:Female; D005978:Glutathione / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism; D006454:Hemoglobins / Q000378:metabolism; D007668:Kidney / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D007674:Kidney Diseases / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008099:Liver / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D008107:Liver Diseases / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D011429:Propolis / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012838:Silymarin / Q000494:pharmacology; D000637:Transaminases / Q000097:blood
D000975:Antioxidants; D001786:Blood Glucose; D006454:Hemoglobins; D012838:Silymarin; D000082:Acetaminophen; D008315:Malondialdehyde; D006003:Glycogen; D011429:Propolis; D003577:Cytochrome P-450 Enzyme System; D002784:Cholesterol; D007770:L-Lactate Dehydrogenase; D000637:Transaminases; D000469:Alkaline Phosphatase; D000135:Acid Phosphatase; D000251:Adenosine Triphosphatases; D005978:Glutathione; D001663:Bilirubin