Research Advances in Cardio-Cerebrovascular Diseases of Ligusticum chuanxiong Hort

Abstract

Cardio-cerebrovascular diseases (CVDs) are a serious threat to human health and account for 31% of global mortality. Ligusticum chuanxiong Hort. (CX) is derived from umbellifer plants. Its rhizome, leaves, and fibrous roots are similar in composition but have different contents. It has been used in Japanese, Korean, and other traditional medicine for over 2000 years. Currently, it is mostly cultivated and has high safety and low side effects. Due to the lack of a systematic summary of the efficacy of CX in the treatment of CVDs, this article describes the material basis, molecular mechanism, and clinical efficacy of CX, as well as its combined application in the treatment of CVDs, and has been summarized from the perspective of safety. In particular, the pharmacological effect of CX in the treatment of CVDs is highlighted from the point of view of its mechanism, and the complex mechanism network has been determined to improve the understanding of CX's multi-link and multi-target therapeutic effects, including anti-inflammatory, antioxidant, and endothelial cells. This article offers a new and modern perspective on the impact of CX on CVDs.

Keywords: Ligusticum chuanxiong Hort.; cardio-cerebrovascular diseases; clinical efficacy; material basis; molecular mechanism.

FIGURE 1

Basic information of Ligusticum chuanxiong Hort. (CX contains tetramethylpyrazine, Z-ligustilide, ferulic acid, and other components, which are widely used in CVDs, including hypertension, CHD, AS, heart failure, cerebral ischemia, and cerebral hemorrhage).

FIGURE 2

Mechanism and pathway of Ligusticum chuanxiong Hort. in the treatment of CVDs.

FIGURE 3

Commonly used drugs for CVD and their mechanisms (the green symbol indicates the effect after administration, and the red symbol indicates the pathological condition. Commonly used drugs for CVDs include statins, BB, ACEI, ARBs, CCB, and nitrates. Angiotensin produced by the liver is converted to Ang I under the action of renin secreted by juxtaglomerular cells, and then to Ang II under the action of ACE. Ang II can bind to AT1 receptor and produce vasoconstriction. BB can bind to β receptor of adjacent glomerular cells and reduce the secretion of renin. ACEI can inhibit ACE and reduce Ang II. ARBs can bind to AT1 receptor and competitively inhibit the binding of Ang II to AT1 receptor. BB, ACEI, and ARBs play a role in the renin–angiotensin system, thereby inhibiting vasoconstriction, reducing blood volume, and lowering blood pressure. CCB can directly block the Ca²⁺ channel on the endothelial cell membrane and reduce Ca²⁺ influx, thereby reducing blood pressure and myocardial contractility. HMG-CoA is transformed into mevalonate by HMG-CoA reductase, and then into cholesterol. Statins can significantly reduce blood cholesterol and LDL by inhibiting HMG-CoA reductase, thus achieving the effect of lowering blood lipid. Nitrates catalyzed the release of NO in the smooth muscle cells by GSTs, and NO activates guanylate cyclase, increasing the content of intracellular second messenger cGMP, and then activating cGMP-dependent protein kinase, which reduces intracellular Ca²⁺ release and extracellular Ca²⁺ influx and relaxes smooth muscle cells).