Echinocystic acid ameliorates hyperhomocysteinemia‑induced vascular endothelial cell injury through regulating NF‑κB and CYP1A1

Abstract

The present study investigated the role of echinocystic acid (EA) on the expression of nuclear factor (NF)-κB and cytochrome P450 1A1 (CYP1A1), and aortic morphology, in a rat model of hyperhomocysteinemia (Hhcy). A total of 50 Sprague Dawley rats were randomly divided into five groups as follows: Normal control (NC), model control (MC), vitamin control (VC; folic acid 1 mg/kg + vitamin B2 2 mg/kg + vitamin B12 10u g/kg), EA1 (20 mg/kg EA) and EA2 (40 mg/kg EA). Plasma homocysteine (Hcy) levels were determined via high performance liquid chromatography, and the morphology of the aorta was investigated using hematoxylin and eosin staining. Furthermore, aortic mRNA and protein levels of NF-κB and CYP1A1 were measured using reverse transcription-quantitative polymerase chain reaction analysis and western blotting, respectively. Plasma Hcy levels, and aortic mRNA and protein levels of NF-κB and CYP1A1, were significantly lower in the EA-treated group compared with the MC group (all P<0.05). However, the aortic morphology remained normal, including the endothelial cells of the inner layer, and smooth muscle cells of the media layer and adventitia. In conclusion, the results of the present study indicate that EA has a protective role on vascular endothelial cells in Hhcy through decreasing plasma Hcy, and thus NF-κB and CYP1A1 expression.

Homocysteine levels, genetic background, and cognitive impairment in Parkinson’s disease

“…Additionally, Hcy can cause damage to vascular endothelial function and alter the permeability of the blood–brain barrier, resulting in small vessel disease in the brain [ 31 ]. Some studies have found that endothelial inflammation under high Hcy conditions promoted vascular injury, which, in turn, led to cognitive impairment [ 32 ].…”

Echinocystic Acid Ameliorates Arthritis in SKG Mice by Suppressing Th17 Cell Differentiation and Human Rheumatoid Arthritis Fibroblast-Like Synoviocytes Inflammation

“…Previous studies revealed that EA alleviated cerebral ischemia/ reperfusion and hyperhomocysteinemia-induced vascular endothelia cell injury via inhibition of the JNK signaling pathway and NF-κB, respectively. 27,47 Additionally, EA suppressed lipopolysaccharide-induced iNOS, TNF-α and IL-6 expressions via NF-κB inactivation in RAW 264.7 macrophages. 48 Of note, the RANKL-induced osteoclastogenesis was inhibited by EA via akin pathways, 49 suggesting that multiple benefits of EA could contribute to the amelioration of RA, including RA-related bony erosion.…”

Relationship Among Homocysteine, Inflammation and Cognitive Impairment in Patients with Acute Ischemic Stroke and Transient Ischemic Attack

“…Combined with the above findings, we speculate that Hcy induces cognitive dysfunction through direct effects on glutamatergic neurotransmission and endothelin, indirect inhibition of methylation processes, enhancement of amyloid neurotoxicity, and promotion of tau phosphorylation. 33 In addition, previous studies have found that endothelial inflammation under high Hcy conditions promoted vascular injury, 34 which in turn led to cognitive impairment. However, the underlying mechanisms remain obscure.…”