Table 3.

The classification of the toxicity action mechanism of aconite and the number of studies.

The toxicity action mechanism of aconite	Occurrence	Reference
The effect on various nerve fiber endings and the central nervous system is initial excitement and then inhibition (the effect of the central nervous system may be related to the promotion of the release of β-endorphin by aconite)	42	Han et al. [10]
Exciting the vagus nerve reduces the autonomy of the sinus node	40	Li [15]
Inhibiting voltage-dependent sodium channels, increasing the sodium ion permeability of nerve cells and myocardial cells, and causing arrhythmia	27	Sheng et al. [5]
Inhibiting the acid cycle of myocardial tricarboxylic and the acidification of oxidative phosphorylation of the respiratory chain, causing myocardial cell damage and necrosis to release myocardial enzymes	19	Strzelecki et al. [16]
Adjusting L-calcium channel activity to relatively prolong repolarization, increasing calcium ion concentration, and causing calcium ion overload in cardiac myocytes	12	Zhou et al. [17]
Exciting cholinergic nerves, inhibiting cholinesterase activity	11	Wang et al. [18]
Inhibiting the vasomotor center	10	Zhang [19]
Inhibiting the Na-K-ATPase activity of the myocardial cell membrane, leading to a large amount of depletion of myocardial high-energy phosphate bonds, and causing damage to myocardial cells	9	Sun et al. [20]
Causing damage to peripheral nerve	7	Wang [21]
Increasing RyR2 protein expression level	4	Peng [22]
β2 adrenergic receptor agonism	4	Lu et al. [23]
Increasing the release of active substances such as prostaglandins and catecholamines	4	Gao and Huang [24]
Promoting the expression of NCX and SERCA2a genes to increase cellular Ca2+ concentration	2	Fu [25]
Causing damage to the DNA of lung fibroblasts	2	Xie [26]
Downregulating gene expression level of Bcl-2 and upregulating gene expression levels of bax	2	Wang et al. [27]
Significantly reducing the mRNA and protein expression levels of PGC-1α in cardiomyocytes	2	Zhao et al. [28]