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Effects of intermedin on autophagy in cerebral ischemia/reperfusion injury
Meng Wang1, Jing Wang2, Zhengang Liu3
1Department of Neurology, North China University of Science and Technology Affiliated Hospital, Tangshan 063000, Hebei Province, China.
Insights
Intermedin (IMD) protects the brain against cerebral ischemia/reperfusion injury by reducing autophagy, similar to 3-methyladenine (3-MA). This finding offers new insights into treating ischemic cerebrovascular diseases.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Cerebral ischemia/reperfusion (I/R) injury (CIRI) is a significant cause of neurological damage.
- Autophagy plays a complex role in the pathophysiology of CIRI, with its precise modulation being a therapeutic target.
Purpose of the Study:
- To investigate the effect of intermedin (IMD) on autophagy in a rat model of cerebral I/R injury.
- To determine if IMD exhibits neuroprotective properties by modulating autophagic pathways.
Main Methods:
- Sixty rats were divided into sham, I/R, IMD, and 3-methyladenine (3-MA) groups.
- Cerebral injury was assessed via neurological function tests, H&E, and TUNEL staining.
- Autophagy markers (LC3, Beclin1, P62) were analyzed using immunohistochemistry and Western blot; ultrastructural changes were examined by transmission electron microscopy.
Main Results:
- Intermedin (IMD) demonstrated a protective effect against CIRI, reducing neuronal damage and infarction, comparable to 3-methyladenine (3-MA).
- IMD treatment led to decreased levels of LC3II/LC3I and Beclin1, and an increased P62 level, indicating autophagy attenuation.
- These molecular changes in the IMD group mirrored the effects observed with 3-MA treatment.
Conclusions:
- Intermedin (IMD) attenuates autophagy, providing neuroprotection against cerebral I/R injury in rats.
- IMD's mechanism of action involves reducing pathological neuronal injury, similar to 3-MA.
- The findings support IMD as a potential therapeutic agent for ischemic cerebrovascular diseases.
Objective:
This study aimed to evaluate the effects of intermedin (IMD) on autophagy in cerebral ischemia/reperfusion (I/R) injury (CIRI).
Methods:
Sixty rats were randomly averaged into four groups: sham, ischemia/reperfusion (I/R), IMD, and 3-methyladenine (3-MA). In the sham group, the right common carotid artery, external carotid artery, and internal carotid artery were detached, and no monofilament was inserted. In the other groups, two hours after cerebral ischemia, the rats were injected through the lateral ventricle with normal saline for I/R group, IMD for the IMD group, and 3-MA for the 3-MA group for 24h. The cerebral injury was assessed by evaluation of neurological function, hematoxylin and eosin (H&E) staining, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. The expressions of autophagy associated proteins, such as microtubule-associated protein 1 light chain 3 (LC3), Beclin1, and sequestosome 1 (P62) were analyzed using immunohistochemistry staining and western blot. Meanwhile, transmission electron microscopy was used to investigate the ultrastructure of the brains.
Results:
IMD could reduce neuron cell damage and infarction formation and has a protective effect against CIRI as 3-MA. The levels of LC3II/LC3I and Beclin1 were significantly decreased and the P62 level was significantly higher in the IMD group compared with I/R group, which is similar to the effect of 3-MA on CIRI.
Conclusions:
IMD has a similar effect as 3-MA, can reduce pathological neuronal injury and protect the brain against CIRI in rats by attenuating the effects of autophagy. Our findings provide evidence for IMD's protective effects in relation to ischemic cerebrovascular diseases.
