Potential therapeutic mechanisms of Draconis Resina in cardiovascular diseases-a narrative review

Abstract

As a traditional Chinese herbal medicine, Draconis Resina (DR) has garnered significant attention due to its efficacy in treating various clinical diseases. Notably, it demonstrates remarkable therapeutic effects in cardiovascular diseases, such as atherosclerosis, coronary heart disease, and myocardial ischemia-reperfusion injury. A comprehensive understanding of the potential therapeutic mechanisms of DR in cardiovascular diseases can positively influence their prevention and treatment. Therefore, through a thorough literature review, this paper summarizes the primary mechanisms of DR in managing cardiovascular diseases, which include the prevention of thrombosis, inhibition of inflammatory responses, alleviation of oxidative stress, enhancement of endothelial function, and mitigation of myocardial fibrosis. There may remain many untapped therapeutic applications of DR that need further exploration. This review aims to give readers a deeper understanding of the DR and offer new perspectives.

Keywords: cardioprotective effect; cardiovascular diseases; draconis resina; loureirin; pharmacology.

Mechanisms of Draconis Resina’s Protection Effects in Cardiovascular Diseases. (NF-κB: Nuclear factor-κB; ROS: Reactive oxygen species; MDA: Malondialdehyde; SOD: Superoxide dismutase; LDH: Lactate Dehydrogenase; MCP-1: Monocyte chemotactic protein - 1; ICAM-1: Intercellular adhesion molecule - 1; VCAM-1: Vascular cell adhesion molecule - 1).

FIGURE 1

PDGF-BB Mediates the Increase of Intracellular Calcium Level to Induce Cell Proliferation and Migration. (PDGF-BB: platelet-derived growth factor-BB; PDGFR: platelet-derived growth factor receptor).

FIGURE 2

Clinical efficacy of draconis resina in the treatment of coronary heart disease in hemorheology, electrocardiogram, cardiac function, markers of myocardial injury and metabolome.

FIGURE 3

The Multiple Pathways of Draconis Resina Treating MIRI. (DR: Draconis Resina; MIRI: Myocardial ischemia-reperfusion injury).

FIGURE 4

The Inhibitory Effect of Draconis Resina on Thrombosis. Draconis Resina inhibits PAI-1 and reduces the binding of PAI-1 to uPA/t-PA, which promotes the conversion of plasminogen into plasmin, thus decreasing the formation of thrombus. (u-PA: Urokinase-type plasminogen activatora; t-PA: Tissue plasminogen activator, PAI-1: Plasminogen activator inhibitor-1).

FIGURE 5

Potential Mechanisms of the Draconis Resina on Cardiovascular Diseases. (A) Prevention of Thrombosis. Plasmin participates in the conversion of fibrinogen to fibrin degradation product. Normally, u-PA and t-PA could promote plasminogen conversion to plasmin. PAI-1 inhibits plasminogen conversion when combined with u-PA or t-PA (left). Loureirin B can reduce the binding of PAI-1 to u-PA or t-PA and promote Plasminogen conversion (right). (B) Inhibition of Inflammatory Responses. DR alleviates inflammation by regulating MAPKs, PPAR, NF-κB, JAK/STAT3, PI3K/AKT/mTOR signaling pathways. (C) Alleviating Oxidative Stress. DR improves oxidative stress by affecting MDA, SOD and LDH levels. (D) Improving Endothelial Function. LTC regulates the MAPK/IKK/IκB/NF-κB signaling pathway to improve endothelial function. (E) Anti-myocardial Fibrosis. DR regulates the TGF-β1/Smad signaling pathway affected by PIN1 and PAI-1 against fibrosis. (AKT: Protein kinase B; DR: Draconis Resina; ICAM-1: Intercellular adhesion molecule - 1; IKK: IκB kinase; IL-1β: Interleukin - 1β; IL-6: Interleukin - 6; IL-8: Interleukin - 8; JAK: Janus kinase; LDH: Lactate dehydrogenase; LPS: Lipopolysaccharide; LTC: Longxue tongluo capsule; MAPK: Mitogen - activated protein kinase; MCP-1: Monocyte chemotactic protein - 1; MDA: Malondialdehyde; mTOR: Mammalian target of rapamycin; NF-κB: Nuclear factor - κB; ox-LDL: Oxidized low - density lipoprotein; PAI-1: Plasminogen activator inhibitor - 1; PI3K: Phosphoinositide 3 - kinase; Pin1: Peptidyl - prolyl cis - trans isomerase NIMA - interacting protein 1; PPAR: Peroxisome proliferator - activated receptor; PTGS: Prostaglandin - endoperoxide synthase; ROS: Reactive oxygen species; SATAT: Signal transducer and activator of transcription; SOD: Superoxide dismutase; TGF-β1: Transforming growth factor - β1; TNFα: Tumor necrosis factor - α; t-PA: Tissue - type plasminogen activator; TβR: Transforming growth factor - β receptor; u-PA: Urokinase - type plasminogen activator; VCAM-1: Vascular cell adhesion molecule - 1).

FIGURE 6

Inflammation in the Artery. (NF-κB: Nuclear factor kappa B, LDL: Low-density lipoprotein; GM-CSF: Granulocyte macrophage colony stimulating factor, M-CSF: Macrophage colony stimulating factor, IL: Interleukin, TNF-α: Tumor necrosis factor-alpha).

FIGURE 7

Oxidative Stress Response in Cardiomyocytes. (LDH: Lactate dehydrogenase, ROS: Reactive oxygen species; MDA: Malondialdehyde, SOD: Superoxide dismutase).

FIGURE 8

Monocyte Adhesion and Thrombosis after Endothelial Dysfunction. (MCP-1: Monocyte chemotactic protein-1, VCAM-1: Vascular cell adhesion molecule-1; ICAM-1: Intercellular adhesion molecule-1).

FIGURE 9

Elevated Myocardial Fibrosis Related Indicators. (TGF-β1: transforming growth factor-β1).