RGD Reference Report - Cimicifuga racemosa impairs fatty acid beta-oxidation and induces oxidative stress in livers of ovariectomized rats with renovascular hypertension. - Rat Genome Database

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Cimicifuga racemosa impairs fatty acid beta-oxidation and induces oxidative stress in livers of ovariectomized rats with renovascular hypertension.

Authors: Campos, LB  Gilglioni, EH  Garcia, RF  Brito Mdo, N  Natali, MR  Ishii-Iwamoto, EL  Salgueiro-Pagadigorria, CL 
Citation: Campos LB, etal., Free Radic Biol Med. 2012 Aug 15;53(4):680-9. doi: 10.1016/j.freeradbiomed.2012.05.043. Epub 2012 Jun 7.
RGD ID: 10449172
Pubmed: PMID:22684021   (View Abstract at PubMed)
DOI: DOI:10.1016/j.freeradbiomed.2012.05.043   (Journal Full-text)

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.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
renovascular hypertension treatmentISOG6pd (Rattus norvegicus)10449172; 10449172 RGD 
renovascular hypertension treatmentIEP 10449172 RGD 

Objects Annotated

Genes (Rattus norvegicus)
G6pd  (glucose-6-phosphate dehydrogenase)

Genes (Mus musculus)
G6pdx  (glucose-6-phosphate dehydrogenase X-linked)

Genes (Homo sapiens)
G6PD  (glucose-6-phosphate dehydrogenase)


Additional Information