Tessaria absinthioides (Hook. & Arn.) DC. (Asteraceae) Decoction Improves the Hypercholesterolemia and Alters the Expression of LXRs in Rat Liver and Hypothalamus

Abstract

Chronic high-fat diet consumption induces hypercholesterolemia. The effect of Tessaria absinthioides (Hook. & Arn.) DC. (Asteraceae) was studied on the levels of total cholesterol (TC), high-density lipoprotein cholesterol (HDL-c), and triglycerides, and on the expression of liver X receptors (LXRs) in a hypercholesterolemic model. Adult male rats received a normal diet (ND) or a high-fat diet (HFD; normal diet + bovine fat + cholesterol). After 14 days, rats received water (W) or a decoction of the aerial parts of T. absinthioides (Ta; 10% w/v) for 2, 4, or 6 weeks. Four and six weeks of Ta improved the levels of TC and HDL-c in HFD. After 6 weeks of Ta, the expression of LXRs in HFD was the same as that in ND in both tissues. The Ta chemical profile was studied with an ultrahigh resolution liquid chromatography Orbitrap MS analysis (UHPLC–PDA–OT-MS/MS). Fifty-one compounds were identified, of which twelve are reported for the first time. Among these compounds, caffeoylquinic acid and its derivatives could modify the lipid profile and the expression of LXRs. This is the first in vivo report of T. absinthioides, which may be a potential candidate against hypercholesterolemia.

Long-Term Memory Function Impairments following Sucrose Exposure in Juvenile versus Adult Rats

“…Animals were fasted for 6 h and blood samples were taken from the tail vein (∼0.5 mL) or from the trunk after decapitation, and immediately centrifuged for 5 min at room temperature (RT) at 1800× g in a tabletop centrifuge. The serum was collected and the levels of TG were measured by spectrophotometry (Wiener Labs S.A.I.C., Rosario, Argentina) as described previously and corticosterone levels were determined by radioimmunoassay using a specific antibody [ 54 , 55 , 56 ].…”

A nexus of lipid and O-Glcnac metabolism in physiology and disease

“…LXR loss in mice does not alter OGA mRNA or OGT protein level but does selectively reduce nuclear O- GlcNAcylation ( 93 ). Protein expression of the LXRα paralog is enhanced by HFD in the rat liver ( 94 – 96 ) and in HepG2 cells by 24 hours in vitro PA ( 96 ). Less data is available on OGA localization patterns but acute OA potentiates the activity of the sOGA isoform and stimulates its accumulation on LD membranes in HeLa cells and 3T3-L1 pre-adipocytes ( 71 ) through an unknown mechanism.…”

“…Furthermore, proteins that target OGT and HBP flux are specifically dysregulated in response to obesity or HFD. Most of the proteins described above are elevated in the liver of obese humans and/or rodents including the protein level and activity of FAS ( 335 – 337 ) and LXRα ( 94 – 96 ). An increase in XBP1 splicing ( 338 ) and p38 activation ( 21 , 339 , 340 ) have also been reported.…”