Cimicifuga racemosa impairs fatty acid β-oxidation and induces oxidative stress in livers of ovariectomized rats with renovascular hypertension.
The aim of this work was to evaluate the effects of therapeutic doses of Cimicifuga racemosa on cardiovascular parameters and on liver lipid metabolism and redox status in an animal model of estrogen deficiency associated with hypertension, a condition that could make the liver more vulnerable to drug-induced injuries. Female Wistar rats were subjected to the surgical procedures of bilateral ovariectomy (OVX) and induction of renovascular hypertension (two-kidneys, one-clip; 2K1C). These animals (OVX + 2K1C) were treated with daily doses of a C. racemosa extract, using a dose that is similar to that recommended to postmenopausal women (0.6 mg/kg), over a period of 15 days. The results were compared to those of untreated OVX + 2K1C, OVX, and control rats. The treatment with C. racemosa caused a significant reduction in blood pressure. In the liver, treatment did not prevent the development of steatosis, and it reduced the mitochondrial and peroxisomal capacity to oxidize octanoyl-CoA compared to the untreated animals. In addition, C. racemosa caused numerous undesirable effects on the liver redox status: it increased the mitochondrial reactive oxygen species generation, an event that was not accompanied by an increase in the activity of superoxide dismutase, and it induced a decrease in peroxisomal catalase activity. Although the reduced glutathione content had not been affected, a phenomenon that probably reflected the restoration of glucose-6-phosphate dehydrogenase activity by C. racemosa, oxidative damage was evidenced by the elevated level of thiobarbituric acid-reactive substances found in the liver of treated animals.
Department of Physiological Sciences, University of Maringá, 87020-900 Maringá, Brazil.
Lilian Brites
LB
Campos
Eduardo Hideo
EH
Gilglioni
Rosângela Fernandes
RF
Garcia
Márcia do Nascimento
Mdo N
Brito
Maria Raquel Marçal
MR
Natali
Emy Luiza
EL
Ishii-Iwamoto
Clairce Luzia
CL
Salgueiro-Pagadigorria
D042962:Acyl-CoA Oxidase / Q000378:metabolism; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology*; D002374:Catalase / Q000378:metabolism; D031885:Cimicifuga / Q000737:chemistry*; D004967:Estrogens / Q000172:deficiency; D005227:Fatty Acids / Q000378:metabolism*; D005234:Fatty Liver / Q000097:blood / Q000188:drug therapy / Q000378:metabolism; D005260:Female; D006978:Hypertension, Renovascular / Q000097:blood / Q000188:drug therapy / Q000378:metabolism*; D050356:Lipid Metabolism; D008055:Lipids / Q000097:blood; D008099:Liver / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D008930:Mitochondria, Liver / Q000378:metabolism; D010052:Ovariectomy; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects*; D010101:Oxygen Consumption; D020675:Peroxisomes / Q000201:enzymology / Q000378:metabolism; D010936:Plant Extracts / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
D000959:Antihypertensive Agents; D004967:Estrogens; D005227:Fatty Acids; D008055:Lipids; D010936:Plant Extracts; D017382:Reactive Oxygen Species; D017392:Thiobarbituric Acid Reactive Substances; D002374:Catalase; D042962:Acyl-CoA Oxidase