Rhodiola rosea was first mentioned in the 8th century Tibetan medicine text "Four Medical Classics." Subsequently, its medicinal value was detailed in "Compendium of Materia Medica" during the Ming Dynasty and in the Tibetan medical classic "Jingzhu Bencao" during the Qing Dynasty. Over time, the medical significance of Rhodiola rosea has become increasingly prominent. In 1977, the "Chinese Pharmacopoeia" formally included Rhodiola rosea, marking its official recognition in modern medicine. It remains listed in the 2020 edition of the "Chinese Pharmacopoeia," further validating its important status in the medical field.

Salidrosides are considered one of the most physiologically active components of Rhodiola rosea. Numerous studies have shown that Salidrosides exhibit a variety of pharmacological effects, including antiviral properties, enhancement of wound healing, cerebral ischemia protection, modulation of neurodegenerative diseases, cardiovascular and liver protection, among others.

Regulation of the Nervous System

Salidrosides exhibit neuroprotective effects, regulate central nervous system neurotransmitters, promote nerve repair, and prevent neuronal apoptosis. Research on the impact of salidrosides on energy metabolism disorders in PC12 cells caused by hypoxia has concluded that these glycosides provide a certain protective effect against hypoxia-induced neuronal damage [1].

Benefits to the Cardiovascular System

Salidrosides offer multiple benefits to the cardiovascular system; they can regulate cardiac function, dilate blood vessels, prevent thrombosis, and possess antioxidant properties. Liu Xinjun et al. found that intraperitoneal injection of salidrosides in mice increased the protein expression and phosphorylation of Akt/GSK-3β in ischemia-reperfusion myocardium, thereby enhancing the protective effect against myocardial ischemia-reperfusion injury [2]. Other studies have concluded that salidrosides exhibit good anti-thrombotic effects both in vitro and in vivo by increasing platelet cAMP levels, reducing platelet TXA2 levels, and inhibiting the PI3K/Akt signaling pathway [3].

Lowering Blood Sugar

Salidrosides can reduce oxidative stress levels in the body, providing certain preventive and protective effects against diabetes; they can also inhibit gluconeogenesis through the AMPK pathway. Additionally, salidrosides may lower blood sugar levels by activating the AMPK signaling pathway to inhibit liver gluconeogenesis [4]. These studies provide a solid theoretical foundation for further exploring the mechanisms by which salidrosides improve diabetes, revealing more potential therapeutic effects.

Anti-Atherosclerosis Effects

Salidrosides also demonstrate significant efficacy in combating atherosclerosis. They can reduce lipid deposition in macrophages and inhibit the formation of foam cells. By suppressing the secretion of inflammatory mediators and cytokines and inhibiting macrophage polarization towards the M1 type, salidrosides may slow down the occurrence and development of atherosclerosis [5].

Anti-Fibrosis Effects in Liver and Lungs

Salidrosides show clear anti-fibrotic effects in liver diseases, effectively protecting hepatocytes, enhancing their regenerative ability, and promoting the recovery of damaged liver cells, thereby reducing local necrotic areas and inhibiting collagen synthesis or promoting ECM degradation. These combined effects help improve liver fibrosis, offering new options for the treatment of liver diseases [6].

Regarding anti-pulmonary fibrosis, salidrosides also exhibit certain effectiveness. They not only inhibit endoplasmic reticulum stress-related proteins during the lung fibrosis process but can also reverse their effects by inhibiting PI3K/AKT pathway activation in fibroblasts, thus reducing endoplasmic reticulum stress activation [7].

References:

[1] Zhong, X. Y. et al (2020). Fujian Journal of Traditional Chinese Medicine. 51(04): 36-38+42.

[2] Liu, X. J. et al. (2015). Journal of Medical Graduate Students. 28(02): 146-148.

[3] Lin X. J. (2019). Guizhou Medical University.

[4] Yuan, S. et al. (2020). Journal of Dalian University. 41(03): 67-71.

[5] Zhou, M. (2018). Yunnan University of Chinese Medicine.

[6] Ouyang, J. F. (2009). Zhejiang University.

[7] Huang, L. et al. (2020). Journal of Guangxi Medical University. 37(08): 1494-1499.