Review of the pharmacological effects of astragaloside IV and its autophagic mechanism in association with inflammation

Table 4 Protective effect of astragaloside IV on diabetes

Disease categories	Study object/model	Effect induced by autophagy	Mechanism (targets or pathways)	Ref.
Diabetic peripheral neuropathy	A high-glucose medium in Schwann cells	Antioxidant activity via (-) the autophagy overactivation of Schwann cells	(-) Reactive oxygen species and (-) autophagy-related proteins (LC3, PINK and Parkin); protective effect (mitochondrial morphology and membrane potential)	Wei et al[38]
Diabetic peripheral neuropathy	High-fat diet in rats; high glucose in Schwann RSC96 cells	(-) The myelin sheath injury by the apoptosis of Schwann cells via (+) autophagy	(-) The activation of the PI3K/Akt/mTOR signalling pathway by (+) miR-155 expression	Yin et al[41]
DN	KK-Ay diabetic mice; immortalized mouse podocytes	(-) Glucose-induced podocyte EMT and (+) enhanced autophagy	The SIRT1–NF-κB pathway	Wang et al[40]
DN	STZ diabetic mice; high glucose in podocytes	(-) The progression of DN via (+) autophagy induction	AMPKα-promoted autophagy induction	Guo et al[39]
Liver injury in diabetics	Highfat diets + lowdose STZ in diabetic liver injury rats	(+) Autophagy in the liver of T2DM rats; (-) IR, dyslipidaemia, oxidative stress and inflammation	The promotion of AMPK/mTORmediated autophagy	Zhu et al[42]

LC: Lung cancer; PINK: PTEN-induced putative kinase 1; RSC: Rat Schwann cells; KK-Ay: Spontaneous diabetes; EMT: Epithelial-mesenchymal transition; STZ: Streptozotocin; DN: Diabetic nephropathy; IR: Immunoreactive; T2DM: Type 2 diabetes mellitus.