|
| Interventions | Key findings | References |
|
| Pharmacological interventions |
| Traditional Chinese medicine (ginsenoside Rb1, puerarin, ginkogolide K, triptolide, and ezetimibe) | (i) Ginsenoside Rb1 ameliorated neuronal injury and increased autophagy after I/R
(ii) Puerarin reduced ischemic brain damage by inhibiting autophagy through the AMPK-mTOR-ULK1 signaling pathway
(iii) GK pretreatment induced autophagy under ischemia and promoted astrocyte proliferation and migration after reoxygenation
(iv) Triptolide decreased apoptosis and induced autophagy, thus conferring neuroprotection
(v) Ezetimibe attenuated neuronal apoptosis by activating autophagy and reduced cerebral cholesterol levels | [8]
[63]
[71]
[72]
[73] |
| Rapamycin | (i) Rapamycin reduced infarct sizes and cell death in both permanent MCAL and embolic MCAO
(ii) Rapamycin may attenuate stroke injury lesion sizes and upregulate autophagy | [64]
[66]
[74]
[19]
[75] |
| Metformin | (i) Acute metformin preconditioning lessened the risk of stroke by enhancing autophagy |
| Nampt | (i) Nampt induced autophagy and promoted cell survival after cerebral ischemia |
|
| Nonpharmacological interventions |
| Electroacupuncture | (i) EA is involved in the initiation of autophagy, vesicle nucleation, and maturation of autophagosomes, in addition to the degradation of autophagolysosomes
(ii) Treatment with EA may influence autophagy activity through regulating autophagy-related proteins | [76]
[77]
[78] |
| Cerebral ischemic pre-/postconditioning or remove ischemic conditioning | (i) Ischemic preconditioning alleviates cerebral I/R injury by activating autophagy, therefore improving neurologic functions
(ii) RIPoC decreased infarct volume, neurological deficits, and cell apoptosis after I/R through regulating autophagy | [79]
[80]
[81]
[82]
[76]
[83]
[84] |
| Hyperbaric oxygen preconditioning (HBO) | (i) HBO preconditioning preserved the integrity of the lysosomal membrane and formed autolysosomes in transient focal cerebral ischemia to activate autophagy
(ii) HBO-mediated autophagy after cerebral I/R was also found to be neuroprotective | [85]
[86]
[87] |
|
| Nucleic acid therapies |
miR-497
miR-30d-5p
miRNA-30a | (i) Cerebral ischemia can lead to abnormal changes in miRNA expression levels involved in the etiology and pathology of stroke
(ii) miR-30a negatively regulates the 3’UTR of Beclin 1 to inhibit autophagy, and miR-30d-5p regulates autophagy in a similar way
(iii) Suppression of miR-497 could increase neuronal autophagy activity to alleviate ischemia injury | [1]
[88]
[89]
[90] |
|
