Table 1.

Protective Mechanism of Curcumin on Blood Vessels

Research Subjects	Intervention Methods	Mechanism	Refs
Ea.hy926 cells	H2O2	By activating the Nrf2/HO-1 signaling pathway	[7]
HUVEC	H2O2	By inhibiting the Notch1 signaling pathway	[8]
HUVEC	H2O2	By increasing antioxidant enzyme activity	[9]
SHR rat	No-intervention	By regulating UCP2/NO signaling pathway, oxidative stress is reduced	[10]
2K-1C hypertensive rats	No-intervention	By reducing MMP levels and inhibiting oxidative stress	[11]
Diabetic mice	No-intervention	Inhibit PKC activity and reduce the production of superoxide	[12]
VECs	Ang II	By inhibiting the expression of CD40	[13]
ApoE−/− mice	High-fat diet	By inhibiting the expression of TLR4 in AS plaques	[14]
HECs	LPS	By down-regulating TLR2, TLR4 and HMGB1 receptors	[15]
HUVECs	HCMV	By inhibiting the HMGB1/TLRS/NF-κB signaling pathway	[16]
HUVECs	Ox-LDL	By regulating the miR-599/MYD88/NF-κB signaling pathway	[17]
ApoE−/− mice	Western diet	By down-regulating LCN2 and inhibiting inflammation	[18]
HECs	Resistin	By inhibiting the expression of p-selectin and fractalkine, NADPH oxidase activation and intracellular ROS levels were decreased	[19]
HAECs	TNF-α	HO-1 expression was induced by activating the p38 MAPK/Nrf2 signaling pathway	[20]
Ea.hy926 cells	TNF-α	By inducing HO-1 expression	[21]
Diabetic rat model	No-intervention	Inhibition of NADPH oxidase, ROS, and ICAM-1 to improve diabetic vascular inflammation	[22]
TAECs	High glucose	By inhibiting the PI3K/Akt/NF-κB signaling pathway	[23]
HUVECs	MGO	By capturing MGO and inhibiting the formation of AGEs	[24,25]
bEnd.3 cells	MGO	By reducing oxidative stress and endoplasmic reticulum stress	[26]
Male Swiss albino mice	AGEs	By neutralizing the AGE-induced inflammatory response	[27]
VECs	Hcy	By inhibiting expression of NF-κB and interleukin-8	[28]
VECs	Acrolein	Inflammation is inhibited by inhibiting PKC/p38 MAPK/CREB pathway	[29]
HAECs	PLLA degraded extracts	By suppressing the inflammatory response	[30]
ApoE−/− mice	HFD	By reducing e-selectin and ICAM-1	[31]
RAECs	High glucose	MCP-1 is reduced by inhibiting the NF-κB pathway	[32]
HUVECs	TNF-α	Curcumin can reduce monocyte adhesion and transendothelial migration	[33]
HUVECs	TNF-α	By inhibiting ROS, LOX-1 and adhesion molecules	]34]
VECs	Radiation	Adhesion molecules are inhibited by regulating the NF-κB and Nrf2 pathways	[35]
LDLR−/− Mice	High-fat diet	By inducing increased cAMP levels in the liver	[36]
SD rat primary hepatocytes	No-intervention	Curcumin increased the level of apoB-48 and decreased the level of ApoB-100 by increasing the expression of APOBEC-1 in rat hepatocytes	[37]
Rats	Splenectomy	Lipid metabolism disorders are improved by regulating NF-κB, SOD and GPx.	[38]
Macrophage	Ox-LDL	By reducing SR-A and increasing ABCA1, cholesterol accumulation is reduced	[39]
THP-1 macrophages	Ox-LDL	ABCA1 is increased by the miR-125a-5p/SI/R T6 signal axis	[40]
RAW 264.7 macrophages	Ox-LDL	The expression of CD36 was inhibited by p38 MAPK signaling pathway	[41]
Macrophages	Ox-LDL	Cholesterol leakage is enhanced by inhibiting the JNK pathway and activating the LXR/ABCA1/SR-BI pathway	[42]
THP-1 macrophages	Ox-LDL	ABCA1 is up-regulated by activation of AMPK/Sirt1 /LXRa signaling pathway	[43]
Macrophage	Ox-LDL	The production of MCP-1 was inhibited by inhibition of JNK and NF-κB pathways	[44]
RAW264.7 macrophages	Ox-LDL	Inhibits the production of inflammatory cytokines such as IL-1β, IL-6, and TNF-α	[45]
Macrophages	HIF-1α	Inhibit inflammation and apoptosis by inhibiting ERK signaling pathway	[46]
RAW264.7 macrophages	No-intervention	Macrophages were polarized to M2 phenotype by activation of PPAR γ	[47]
Macrophages	LPS and IFN-γ	Inhibition of TLR4/MAPK/NF-κB pathway promotes the transformation of M1 macrophages to M2 phenotype	[48]
ApoE−/− mice	Cadmium	By regulating intestinal flora, lipid metabolism imbalance and M1-type macrophage polarization were improved	[49]
Macrophages	Ox-LDL	The expression of EMMPRIN and MMP-9 was inhibited by down-regulating NF-κB and p38 MAPK signaling pathways	[50]
THP-1 macrophages	PMA	The expression of EMMPRIN, MMP-9 and MMP-13 was inhibited by PKC and AMPK pathways	[51]
Macrophages	Ox-LDL	By inhibiting the decrease of THBS-4 expression	[52]
EPCs	High glucose	By increasing MnSOD, EPCs dysfunction induced by high glucose is alleviated	[53]
EPCs	EPC isolated from diabetic mice	By up-regulating the expression of VEGF-A and Ang1, the migration and proliferation of EPCs were promoted	[54]
SD rat	Balloon injury carotid endothelium	By inducing autophagy, inhibiting oxidative stress and apoptosis	[55]
HUVECs	Ischemia	Promote angiogenesis by upregulating miR-93	[56]
Rats	CsA	Alleviating CsA-induced endothelial dysfunction in rats by anti-oxidative stress	[57]
Male Wistar rat	Methotrexate	Eliminate vascular side effects of methotrexate by inhibiting oxidative stress and reducing physiological NO levels	[58]
RAECs	Rapamycin	Antagonizing the harmful effect of rapamycin on RAECs by upregulating eNOS	[59]
Laboratory pig	PLLA stents	Alleviating foam cell inflammation caused by PLLA degradation through PPAR γ signaling pathway	[60]
HMEC	PM2.5	By reducing the levels of ROS, ox-LDL, ICAM-1 and VCAM-1	[61]
HUVEC	Palmitic acid	The upregulation of LOX-1 is blocked by inhibiting ERS, thereby reducing subcutaneous lipid deposition	[62]
HUVEC	H2O2	Autophagy is promoted by inhibiting the PI3K/Akt/mTOR signaling pathway	[63]
Ea.hy926 cells	H2O2	Autophagy is induced by Akt/mTOR pathway, thereby alleviating apoptosis	[64]
HUVECs	Ox-LDL	By modulating AMPK/mTOR/p70S6K autophagy signaling pathway	[65]
Human monocytic THP-1 cells	Ox-LDL	Curcumin regulates ox-LDL-induced macrophage autophagy and inflammation via the TFEB/P300/BRD4 pathway	[66]
Macrophages	PMA	NLRP3 inflammasome of macrophage was decreased by inhibiting TLR4/MyD88/NF-κB signaling	[67]
HUVEC	H2O2	Inhibition of H2O2-induced HUVEC pyrodeath by inhibiting NLRP3 activation	[68]
HUVECs	H2O2	Oxidative stress-induced HUVECs senescence was alleviated by activating Sirt1	[69]
HUVECs	TGF-β1	Curcumin inhibits EndMT by regulating the RF2/DDAH/ADMA/NO pathway	[70]
Mesenteric artery endothelial cells	Phenylephrine	Activation of TRPV4 channels stimulates Ca2+ entry into endothelial cells, thereby improving vasodilation function	[71]
SHR rats	Ang II	VSMCs migration is mitigated by inhibiting the NF-κB/NLRP3 signaling pathway	[72]
SD rats	Arterial balloon injury	The proliferation and migration of VSMCs after arterial balloon injury was inhibited by regulating the miR-22/SP1 pathway	[73]
ApoE−/− mice	HFD	Inhibition of chemerin/CMKLR1/LCN2 pathway mitigated the proliferation and migration of VSMCs during AS	[74]
VSMCs	IGF-1	By inhibiting PKB/GSK-3β/Egr-1 pathway, IGF-1-induced VSMCs proliferation and migration were attenuated	[75]
VSMCs	TNF-α	The expression and activity of MMP-2 were inhibited by NF-κB pathway, thereby inhibiting the migration of VSMCs	[76]
VSMCs	LPS	MMP-2 activity was inhibited by Ras/MEK1/2 pathway	[77]
VSMCs	Endothelin	By increasing PPAR γ activity and inhibiting NADPH oxidase, the release of inflammatory factors from VSMCs was inhibited	[78]
VSMCs	Aldosterone	Inhibiting CRP production in VSMCs by interfering ROS/ERK1/2 signaling	[79]
VSMCs	LPS	Inhibition of inflammatory mediators in VSMCs via TLR4/MAPK/NF-κB pathway	[80]
VSMCs	Ox-LDL	The expression of MCP-1 in VSMCs was inhibited by inhibiting p38MAPK and NF-κB pathways	[81]
VSMCs	LPS	Reducing VSMC inflammation by inhibiting NF-κB and JNK signaling pathways	[82]
C57Bl/6J mice	Ang II	The expression of AT1R in VSMCs was down-regulated by inhibiting SP1/AT1R DNA binding	[83]
VSMCs	ET-1	By inhibiting c-Raf/ERK1/2/Egr-1 and IGF-1R/PKB pathways	[84]
VSMCs	AngII	The transition of VSMC from systolic to synthetic is inhibited by regulating the PTEN/Akt pathway	[85]