Atrial Fibrillation in Cardiosurgical Patients

Sapelnikov, O.V.; Latypov, R. S.; Partigulova, A.; Shiryaev, А. A.; Акчурин, Р. С.

doi:10.18565/cardio.2015.11.5-11

Cited by 1 publication

(2 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Regulation of intracellular sodium balance and volume of extracellular fluid is maintained by the RAAS. Inflammatory process and subsequent tissue damage leading to development of fatty streaks, foam cell formation and ultimately to formation of rupture susceptible plaques is also associated with RAAS [44–46] . In the present study induction of atherosclerosis in mice caused a prominent increase in expression of AngII, AT1 and AT2 proteins in aorta tissues.…”

Section: Discussionsupporting

confidence: 54%

“…Inflammatory process and subsequent tissue damage leading to development of fatty streaks, foam cell formation and ultimately to formation of rupture susceptible plaques is also associated with RAAS. [44][45][46] In the present study induction of atherosclerosis in mice caused a prominent increase in expression of AngII, AT1 ChemistrySelect and AT2 proteins in aorta tissues. However, treatment of the atherosclerosis mice with berberine caused a remarkable reduction in AngII, AT1 and AT2 protein expression compared to the mode group.…”

Section: Chemistryselectmentioning

confidence: 95%

See 1 more Smart Citation

Berberine Exhibits Anti‐atherosclerotic Effects in a Mouse Model by Targeting the JAK/STAT Pathway

et al. 2023

View full text Add to dashboard Cite

Atherosclerosis, a serious and commonly diagnosed pathological condition is the main cause of coronary and cerebrovascular disorder which has a high rate of morbidity and mortality globally. In the present study effect of berberine on damage to the aorta wall induced by atherosclerosis in mice model was investigated. The results demonstrated that berberine treatment significantly (P<0.05) reverses the atherosclerosis‐induced increase in the area of the lesions in the mice aortas. Berberine treatment at 0.5, 1.0 and 2.0 mg/kg doses reduced lesion area in the aorta of atherosclerosis mice to 53.5±3.69, 39.4±3.69 and 13.8±2.12 %, respectively. Atherosclerosis‐induced up‐regulation of interleukin (IL)‐1β and IL‐6 production was down‐regulated in mice aortas on treatment with berberine. Treatment with berberine downregulated the atherosclerosis‐induced increase in expression of monocyte chemoattractant protein‐1 (MCP‐1), tumor necrosis factor (TNF)‐α, angiotensin II (AngII), Alveolar type 2 progenitor cells (AT1), and AT2 in mice aorta tissues. Moreover, berberine treatment of atherosclerosis mice led to a marked reduction in the activation of signal transducer and activator of transcription 3 (STAT3), p65, and p38 proteins. In summary, berberine treatment reverses damage associated with atherosclerosis in mice aorta walls by inhibiting the inflammatory response. It targets activation of Janus kinase (JAK)/STAT pathway and downregulated RAAS expression in atherosclerotic mice. Therefore, berberine may be developed as a potential chemotherapeutic agent for atherosclerosis treatment.

show abstract

Section: Discussionsupporting

confidence: 54%

Section: Chemistryselectmentioning

confidence: 95%