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Eur Rev Med Pharmacol Sci. 2019 Sep;23(18):8168-8174. doi: 10.26355/eurrev_201909_19037.

Effect of levocarnitine on cerebral ischemia-reperfusion rats via activating Nrf2/ARE signaling pathway.

Author information

1
Department of Neurology, Linyi Central Hospital, Linyi, Shandong, China. zyc19851103@163.com.

Abstract

OBJECTIVE:

Levocarnitine plays a crucial role in the metabolism of organisms. The aim of this study was to explore the impact of Levocarnitine on cerebral ischemia-reperfusion (I/R) rats and the underlying mechanism.

MATERIALS AND METHODS:

Cerebral I/R model was first successfully established. Two groups were set up, including drug group (I/R + Levocarnitine group) and control group (I/R group). The influences of Levocarnitine on brain injury and oxidative stress in cerebral I/R rats were evaluated. Furthermore, the impacts of Levocarnitine on the nuclear factor E2-related factor 2 (Nrf2)/antioxidant responsive element (ARE) signaling pathway and neuronal apoptosis in rats were detected.

RESULTS:

Compared with I/R group, I/R + Levocarnitine group exhibited markedly lowered neurological deficit score and cerebral infarct volume. However, superoxide dismutase (SOD) and notably decreased malondialdehyde (MDA) were significantly up-regulated in I/R + Levocarnitine group. This suggested that Levocarnitine could relieve cerebral nerve injury and oxidative stress in cerebral I/R rats. Additionally, in I/R + Levocarnitine group, the protein expressions of Nrf2, heme oxygenase-1 (HO-1), and B-cell lymphoma 2 (Bcl-2) were significantly up-regulated, whereas cleaved Caspase-3 (c-Caspase-3) was notably down-regulated. Furthermore, neuronal apoptosis in cerebral I/R rats was remarkably inhibited.

CONCLUSIONS:

Levocarnitine alleviates brain injury and neuronal apoptosis in cerebral I/R rats by activating the Nrf2/ARE signaling pathway.

PMID:
31599449
DOI:
10.26355/eurrev_201909_19037
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