Fufang-Zhenzhu-Tiaozhi capsule ameliorates rabbit’s iliac artery restenosis by regulating adiponectin signaling pathway

Atherosclearosis plaque formation is related to EndMT in diabetic minipigs with coronary heart disease and the effect of Traditional Chinese medicine FTZ Prescription

“…In the cardiovascular aspect, FTZ has the cardioprotective effect in the treatment of DM-CHD and diabetic cardiomyopathy (DCM) through inhibiting ERK and STAT3 signal pathways and activating PI3K/AKT pathway [24,49]. Furthermore, recent studies have shown that FTZ reduced restenosis in the rabbit restenosis model by regulating the adiponectin pathway and reducing NF-κB activity [21,22], but the effect of FTZ on vascular endothelium has not been explicit. In this study, we found that FTZ signi cantly inhibited the EndMT of coronary artery in DM-CHD minipigs and revised the reduced cell viability of HUVECs caused by HG.…”

“…Previous studies have shown that FTZ could inhibit the development of atherosclerosis in the atherosclerosis model and exhibit the cardioprotective effect in the diabetic minipig model with coronary heart disease (DM-CHD) [21][22][23][24]. However, the effect and molecular mechanisms underlying FTZ in DM-CHD are not clear.…”

The Traditional Chinese Medicine Formula FTZ Protects against Cardiac Fibrosis by Suppressing the TGFβ1-Smad2/3 Pathway

“…Results from our preliminary in vivo studies demonstrated that FTZ could ameliorate several pathological processes such as inflammation, abnormal blood coagulation, endothelial dysfunction, and the formation of atherosclerotic plaques. In addition, FTZ can regulate glucose and lipid metabolism and reduce oxidative stress in rodent models [ 9 – 11 ]. More importantly, a recent study reported that FTZ could ameliorate diabetic cardiomyopathy by inhibiting inflammation and cardiac fibrosis [ 12 ]; however, its mechanism in inhibiting cardiac fibrosis was unclear.…”

FTZ Ameliorates Diabetic Cardiomyopathy by Inhibiting Inflammation and Cardiac Fibrosis in the Streptozotocin-Induced Model

“…Our serial studies have identified the main components and potential targets of FTZ and demonstrated its protective effects in treating hyperlipidemia, diabetes, nonalcoholic fatty liver disease (NAFLD), and aging-induced osteoporosis through regulation of HMG-CoA reductase (HMGCR) and cholesterol 7-alpha hydroxylase (CYP7A1), attenuating insulin resistance, inhibiting the formation and activation of the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome, and modulating sphingolipid, glycerophospholipid, and amino acid metabolisms, respectively [11,[14][15][16]. With the ability to alleviate inflammation and improve vascular endothelium function, FTZ is a promising drug for the treatment of cardiovascular diseases [17]. Previous studies have shown that FTZ could inhibit the development of atherosclerosis by reducing the degree of vascular restenosis in the atherosclerosis model by regulating the adiponectin signaling pathway and inhibiting the expression of inflammatory factors [17][18][19].…”

“…With the ability to alleviate inflammation and improve vascular endothelium function, FTZ is a promising drug for the treatment of cardiovascular diseases [17]. Previous studies have shown that FTZ could inhibit the development of atherosclerosis by reducing the degree of vascular restenosis in the atherosclerosis model by regulating the adiponectin signaling pathway and inhibiting the expression of inflammatory factors [17][18][19]. However, the effect and molecular mechanisms underlying FTZ in cardiac diseases, especially in DCM have not yet been widely reported.…”