Astragalus and its formulas as a therapeutic option for fibrotic diseases: Pharmacology and mechanisms

Abstract

Fibrosis is the abnormal deposition of extracellular matrix, characterized by accumulation of collagen and other extracellular matrix components, which causes organ dysfunction and even death. Despite advances in understanding fibrosis pathology and clinical management, there is no treatment for fibrosis that can prevent or reverse it, existing treatment options may lead to diarrhea, nausea, bleeding, anorexia, and liver toxicity. Thus, effective drugs are needed for fibrotic diseases. Traditional Chinese medicine has played a vital role in fibrotic diseases, accumulating evidence has demonstrated that Astragalus (Astragalus mongholicus Bunge) can attenuate multiple fibrotic diseases, which include liver fibrosis, pulmonary fibrosis, peritoneal fibrosis, renal fibrosis, cardiac fibrosis, and so on, mechanisms may be related to inhibition of epithelial-mesenchymal transition (EMT), reactive oxygen species (ROS), transforming growth factor beta 1 (TGF-β1)/Smads, apoptosis, inflammation pathways. The purpose of this review was to summarize the pharmacology and mechanisms of Astragalus in treating fibrotic diseases, the data reviewed demonstrates that Astragalus is a promising anti-fibrotic drug, its main anti-fibrotic components are Calycosin, Astragaloside IV, Astragalus polysaccharides and formononetin. We also review formulas that contain Astragalus with anti-fibrotic effects, in which Astragalus and Salvia miltiorrhiza Bunge, Astragalus and Angelica sinensis (Oliv.) Diels are the most commonly used combinations. We propose that combining active components into new formulations may be a promising way to develop new drugs for fibrosis. Besides, we expect Astragalus to be accepted as a clinically effective method of treating fibrosis.

Preclinical Investigations on Anti-fibrotic Potential of Long-Term Oral Therapy of Sodium Astragalosidate in Animal Models of Cardiac and Renal Fibrosis

“…The activation of the Smads pathway and its subsequent nuclear translocation are critical steps in TGF-β1-mediated fibrosis. 19 In our study, the protein expression of TGF-β1 and Smads in kidney tissues was detected via Western blot (Figure 5). When compared with db/m mice, as expected, the protein expression of TGF-β1 and Smad2/3 was significantly increased and that of Smad7 was decreased in the db/db mice (Figure 5A−C).…”

“…The activation of the Smads pathway and its subsequent nuclear translocation are critical steps in TGF-β1-mediated fibrosis . In our study, the protein expression of TGF-β1 and Smads in kidney tissues was detected via Western blot (Figure ).…”

From Basic Research to Clinical Practice: Considerations for Treatment Drugs for Silicosis

“…Oxidation, and imbalance in oxidation, can be attributed to the fluctuations in the levels of antioxidant enzymes linked to pulmonary fibrosis, as well as ROS catalyzed by NOX2/4. Studies have revealed that white tea extract and astragalus could enhance the level of antioxidant enzymes in lung tissue, strengthen the antioxidant capacity of lung tissue, and exhibit antifibrotic properties [59].…”

Astragaloside-IV promotes autophagy via the Akt/mTOR pathway to improve cellular lipid deposition

“…It is widely utilized as an alternative treatment for immunological diseases, metabolic diseases, and liver fibrosis. [11][12][13] Astragaloside IV (AS-IV), the main active substance of Astragalus membranaceus, with the molecular formula of C 41 H 68 O 14 , can inhibit the abnormal expression of lipid synthesis-related genes, improve the ability to resist oxidative stress, reduce the degree of endoplasmic reticulum stress, decrease inflammatory response, and inhibit apoptosis. [14][15][16] AS-IV can improve liver lipid deposition in mice with NAFLD.…”