Protective effect of oleanolic acid on oxidized-low density lipoprotein induced endothelial cell apoptosis

Cao, Jianhua; Li, Guanghui; Wang, Meizhi; Li, Hui; Han, Ze‐Guang

doi:10.5582/bst.2015.01094

Cited by 7 publications

(3 citation statements)

References 36 publications

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“…Ox-LDL can enhance ROS generation in endothelial cells 44 45 and macrophages 46 47 . Fructose consumption induces high serum ox-LDL levels observed in adult or children subjects 2 7 , as well as in rats in the present study ( Table 2 ).…”

Section: Resultsmentioning

confidence: 99%

Cinnamaldehyde and allopurinol reduce fructose-induced cardiac inflammation and fibrosis by attenuating CD36-mediated TLR4/6-IRAK4/1 signaling to suppress NLRP3 inflammasome activation

Kang

Zhang

et al. 2016

Sci Rep

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Fructose consumption induces metabolic syndrome to increase cardiovascular disease risk. Cinnamaldehyde and allopurinol possess anti-oxidative and anti-inflammatory activity to relieve heart injury in metabolic syndrome. But the mechanisms of fructose-induced cardiac injury, and cardioprotective effects of cinnamaldehyde and allopurinol are not completely understood. In this study, fructose-fed rats displayed metabolic syndrome with elevated serum ox-LDL, cardiac oxidative stress, inflammation and fibrosis. Scavenger receptor CD36, Toll-like receptor 4 (TLR4), TLR6, IL-1R-associated kinase 4/1 (IRAK4/1), nucleotide-binding domain (NOD)-like receptor protein 3 (NLRP3) inflammasome, interleukin-1β, transforming growth factor-β (TGF-β), drosophila mothers against DPP homolog (Smad) 2/3 phosphorylation and Smad4 were increased in animal and H9c2 cell models. These pathological processes were further evaluated in ox-LDL or fructose-exposed H9c2 cells pretreated with ROS scavenger and CD36 specific inhibitor, or IRAK1/4 inhibitor, and transfected with CD36, NLRP3, or IRAK4/1 siRNA, demonstrating that NLPR3 inflammasome activation through CD36-mediated TLR4/6-IRAK4/1 signaling may promote cardiac inflammation and fibrosis. Cinnamaldehyde and allopurinol reduced cardiac oxidative stress to suppress NLPR3 inflammasome activation and TGF-β/Smads signaling by inhibiting CD36-mediated TLR4/6-IRAK4/1 signaling under fructose induction. These results suggest that the blockage of CD36-mediated TLR4/6-IRAK4/1 signaling to suppress NLRP3 inflammasome activation by cinnamaldehyde and allopurinol may protect against fructose-induced cardiac inflammation and fibrosis.

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Section: Resultsmentioning

confidence: 99%

Cinnamaldehyde and allopurinol reduce fructose-induced cardiac inflammation and fibrosis by attenuating CD36-mediated TLR4/6-IRAK4/1 signaling to suppress NLRP3 inflammasome activation

Kang

Zhang

et al. 2016

Sci Rep

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show abstract

“…[ 13,21,23 ] Additionally, HIF‐1 activates BAMBI, which is proved to be an essential modulator for TGF‐β pathway. [ 24 ] Interestingly, ox‐LDL treatment increases HIF‐1α expression in HUVECs, [ 25 ] but BAMBI expression keeps unchanged. [ 13 ] These studies suggest that there may be other upstream modulators of BAMBI in ECs.…”

Section: Discussionmentioning

confidence: 99%

miR‐125a‐3p aggravates ox‐LDL‐induced HUVEC injury through BAMBI

Xia

Zeng

2022

J Biochem & Molecular Tox

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Atherosclerosis (AS) is a chronic inflammatory disease characterized by the formation of atherosclerotic plaque in the intima of arteries. Among the known regulators of atherosclerosis, microRNAs (miRNAs) have been reported to play critical roles in lipoprotein homeostasis and plaque formation. But the roles of microRNA‐125a‐3p (miR‐125a‐3p) in the pathogenesis of AS remain unknown. Human umbilical vein endothelial cells (HUVECs) were treated with oxidized low‐density lipoprotein (ox‐LDL) to construct the vascular injury model of AS pathogenesis in vitro. miR‐125a‐3p and BMP and activin membrane‐bound inhibitor (BAMBI) expression levels in HUVECs were then measured by quantitative real‐time polymerase chain reaction and western blot. The viability and apoptosis of HUVECs were analyzed by Cell Counting Kit‐8 assay, TUNEL assay, and flow cytometry, respectively. The relationship between BAMBI 3′‐untranslated region and miR‐125a‐3p was validated by dual luciferase reporter gene assay. miR‐125a‐3p expression was raised in HUVECs induced with ox‐LDL. In HUVECs, miR‐125a‐3p enhanced the effects of ox‐LDL treatment on repressing the viability and promoting the apoptosis of cells. Additionally, BAMBI was confirmed as a direct target of miR‐125a‐3p and BAMBI overexpression reversed the effects of miR‐125a‐3p on HUVECs. miR‐125a‐3p aggravates the dysfunction of HUVECs induced by ox‐LDL via BAMBI, which implies that miR‐125a‐3p is involved in the pathogenesis of AS.

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“…Oxidative stress was deemed the critical mechanism in AS [ 133 ]. Research demonstrated that OA may safeguard HUVECs damage by inhibiting the levels of lipoprotein receptor 1 (LOX-1), ROS, as well as hypoxia-inducible factor 1 α (HIF-1α) [ 134 ]. Moreover, OA has been confirmed to alleviate HUVECs damage via the reduction in the level of ROS and LOX-1, as well as enhancing the level of Nrf2/HO-1 [ 135 ].…”

Section: Anti-cardiovascular Diseases Effectsmentioning

confidence: 99%

The Effect and Mechanism of Oleanolic Acid in the Treatment of Metabolic Syndrome and Related Cardiovascular Diseases

Luo,

Wei,

et al. 2024

Molecules

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Metabolic syndromes (MetS) and related cardiovascular diseases (CVDs) pose a serious threat to human health. MetS are metabolic disorders characterized by obesity, dyslipidemia, and hypertension, which increase the risk of CVDs’ initiation and development. Although there are many availabile drugs for treating MetS and related CVDs, some side effects also occur. Considering the low-level side effects, many natural products have been tried to treat MetS and CVDs. A five-cyclic triterpenoid natural product, oleanolic acid (OA), has been reported to have many pharmacologic actions such as anti-hypertension, anti-hyperlipidemia, and liver protection. OA has specific advantages in the treatment of MetS and CVDs. OA achieves therapeutic effects through a variety of pathways, attracting great interest and playing a vital role in the treatment of MetS and CVDs. Consequently, in this article, we aim to review the pharmacological actions and potential mechanisms of OA in treating MetS and related CVDs.

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Protective effect of oleanolic acid on oxidized-low density lipoprotein induced endothelial cell apoptosis

Cited by 7 publications

References 36 publications

Cinnamaldehyde and allopurinol reduce fructose-induced cardiac inflammation and fibrosis by attenuating CD36-mediated TLR4/6-IRAK4/1 signaling to suppress NLRP3 inflammasome activation

Cinnamaldehyde and allopurinol reduce fructose-induced cardiac inflammation and fibrosis by attenuating CD36-mediated TLR4/6-IRAK4/1 signaling to suppress NLRP3 inflammasome activation

miR‐125a‐3p aggravates ox‐LDL‐induced HUVEC injury through BAMBI

The Effect and Mechanism of Oleanolic Acid in the Treatment of Metabolic Syndrome and Related Cardiovascular Diseases

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