Tanshinone IIA attenuates elastase-induced AAA in rats via inhibition of MyD88-dependent TLR-4 signaling

Abstract

Tan IIA attenuates elastase-induced AAA in rats possibly via the inhibition of MyD88-dependent TLR-4 signaling, which may be one potential explanation of why Tan IIA inhibits AAA development through multiple effects.

Toll-like receptor-4 signaling pathway in aorta aging and diseases: “its double nature”

“…TLR-4 is recognized to have a key function in the host defence against Gram-negative bacteria, viruses, fungi and mycoplasma [10], but also in the patho-physiology of several age-related diseases [9,11], including CVDs, as stressed in our studies [4,8,11,12] and described by other groups [13][14][15]. Recently, its role has emerged in maintaining aortic homeostasis, but also in establishing aorta aneurysm [4,8,[16][17][18][19][20][21][22][23][24][25][26][27][28][29].…”

“…In fact, the role of TLR-4 mediated receptor signaling pathway in the context of aorta diseases is also emerging [16][17][18][19][20][21][22][23][24][25][26][27][28][29]. In particular, our group postulates its fundamental contribution to the development of sporadic TAA, as reported in the above mentioned model [4,8].…”

DNA Methylation Regulates Gene Expression in Intracranial Aneurysms

“…18 Moreover, by inhibiting the TLR4/MyD88 signaling pathway, tansh in one type IIA can reduce the formation of an AAA induced by elastase. 19 In this study, the expression ofTLR4 mRNA in the intracranial aneurysm tissue was higher than that in the superficial temporal artery, and the methylation of the TLR4 gene was down-regulated (i.e., the methylation level at the cg13730105 and cg05429895 TLR4 sites decreased by 0.17 and 0.28, respectively). The suppression of TLR4 methylation increasedTLR4 transcription and activated NF-κB signaling pathways, leading to the occurrence and development of aneurysms.…”

Study of the functional mechanisms of osteopontin and chemokine-like factor 1 in the development and progression of abdominal aortic aneurysms in rats

“…At present, scholars at home and abroad have created AAA rat models through a range of methods including genetic defect induction, calcium chloride-mediated injury and elastase perfusion (9). Among these methods, the elastase perfusion model is superior in mimicking the native pathological conditions in AAA patients (10). In the present study, the AAA rat model was successfully generated using a micro-surgery method.…”