The Significant Therapeutic Effects of Chinese Scorpion: Modern Scientific Exploration of Ion Channels

Abstract

Chinese scorpion (CS), a traditional animal-based medicine used for over a millennium, has been documented since AD 935-960. It is derived from the scorpion Buthus martensii Karsch and is used to treat various ailments such as stroke, epilepsy, rheumatism, and more. Modern research has identified the pharmacological mechanisms behind its traditional uses, with active components like venom and proteins showing analgesic, antitumor, antiepileptic, and antithrombotic effects. Studies reveal that CS affects ion channels, crucial for cellular functions, through interactions with sodium, potassium, and calcium channels, potentially explaining its therapeutic effects. Future research aims to elucidate the precise mechanisms, target specific ion channel subtypes, and validate clinical efficacy and safety, paving the way for novel therapies based on these natural compounds.

Keywords: Buthus martensii Karsch; chemical components; ion channel; pharmacological effects.

Figure 7

Structures of special small-molecule compounds in CS.

Figure 1

The interaction of scorpion toxins with specific ion channels elicits antitumor effects. (A) Modulation of cellular targets involved in cancer cell proliferation and apoptosis mechanisms by sodium channels scorpion toxins. (B) Inhibition of cellular targets involved in cancer cell proliferation and migration mechanisms by potassium channels scorpion toxins. (C) Inhibition of cellular targets involved in cancer cell invasion and migration mechanisms by chloride channel scorpion toxins [12] (reproduced with permission from Najet Srairi-Abid, Cell Calcium; published by Elsevier, 2019).

Figure 2

Mode of action for peptides with analgesic activity [22] (reproduced with permission from Zhongjie Li, Peptides; published by Elsevier, 2019).

Figure 3

Diagram illustrating the pathways associated with AGAP. (A) AGAP induces analgesia by effectively alleviating acute inflammatory pain and chronic constrictive injury through the modulation of MAPK and Fos signaling pathways in formalin-induced models. (B) AGAP decreases breast cancer cell stemness and epithelial–mesenchymal transition. (C) AGAP influences SHG-44 human malignant glioma cells and colon cancer cells [24] (reproduced with permission from Seidu A. Richard, Evidence-Based Complementary and Alternative Medicine; published by Hindawi, 2020).

Figure 4

The structure of potassium channels [40] (reproduced with permission from Chenglai Xia, Biomedicine & Pharmacotherapy; published by Elsevier, 2023).

Figure 5

Proposed mechanism for the interaction between BK channels (α + β4) and martentoxin. The conformation of a normal open state (A) was changed by the application of martentoxin when the first steady complex was formed (B). Then, the low-affinity site was exposed to associate with martentoxin (C) or iberiotoxin (D) [62] (reproduced with permission from Yonghua Ji, Biophysical Journal; published by Elsevier, 2008).

Figure 6

Mode of action of martentoxin and bumarsin. KCa: Ca²⁺-activated K⁺ channels; iNOS: inducible nitric oxide synthase; NO: nitric oxide [22] (reproduced with permission from Zhongjie Li, Peptides; published by Elsevier, 2019).

Figure 8

Sequence alignment of the 22 identified full-length scorpion toxins. Similarities in sequences are indicated with shading. The six conserved cysteine residues in all toxins, capable of forming three disulfide bonds, are illustrated by the red box with connecting lines [92] (reproduced with permission from Yingliang Wu, Journal of Proteomics; published by Elsevier, 2019).