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The Role of Omega-3 Polyunsaturated Fatty Acids in Stroke.

Bu J, Dou Y, Tian X, Wang Z, Chen G - Oxid Med Cell Longev (2016)

Bottom Line: Evidence is accumulating that the dietary supplementation of fish oil exhibits beneficial effects on several diseases, such as cardiovascular diseases, metabolic diseases, and cancer.Omega-3 polyunsaturated fatty acids (n-3 PUFAs), the major component of fish oil, have been found against oxidative stress and inflammation in cardiovascular diseases.In this review, we will review the effects of n-3 PUFAs on stroke and mainly focus on the antioxidant and anti-inflammatory effects of n-3 PUFAs.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou 215006, China.

ABSTRACT
Stroke is the third commonest cause of death following cardiovascular diseases and cancer. In particular, in recent years, the morbidity and mortality of stroke keep remarkable growing. However, stroke still captures people attention far less than cardiovascular diseases and cancer. Past studies have shown that oxidative stress and inflammation play crucial roles in the progress of cerebral injury induced by stroke. Evidence is accumulating that the dietary supplementation of fish oil exhibits beneficial effects on several diseases, such as cardiovascular diseases, metabolic diseases, and cancer. Omega-3 polyunsaturated fatty acids (n-3 PUFAs), the major component of fish oil, have been found against oxidative stress and inflammation in cardiovascular diseases. And the potential of n-3 PUFAs in stroke treatment is attracting more and more attention. In this review, we will review the effects of n-3 PUFAs on stroke and mainly focus on the antioxidant and anti-inflammatory effects of n-3 PUFAs.

No MeSH data available.


Related in: MedlinePlus

The Nrf2/HO-1 signaling pathway induced by n-3 PUFAs.
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Related In: Results  -  Collection


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fig2: The Nrf2/HO-1 signaling pathway induced by n-3 PUFAs.

Mentions: The dietary supplementation of n-3 PUFAs can decrease the volume of cerebral infarction partly by adjusting antioxidant enzymes activities and partly by working as an antioxidant directly [35]. n-3 PUFAs may act as an antioxidant in reducing cerebral lipid peroxides and play a role in regulating oxidative stress through the increase of oxidative burden and the improvement of antioxidative defense capacity [36]. The chronic administration and dietary supplementation of n-3 PUFAs can improve symptoms of cerebral I/R by increasing the antioxidative capacity, as well as reducing the induction of chaperon molecules and the stabilization of membrane integrity and lipid peroxidation [37]. The dietary supplementation of ALA is also found such that it can reduce the level of lipid peroxidation, as well as increasing the risk of spontaneous reperfusion [38]. The neuroprotective effects of n-3 PUFAs include not only inhibiting the oxidative stress but also enhancing the expression of nuclear factor E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) [39]. The Nrf2/HO-1 signaling pathway induced by n-3 PUFAs is shown in Figure 2. Nrf2/HO-1 signaling pathway is a crucial mechanism of n-3 PUFAs for protecting cells [40]. n-3 PUFAs reduce ischemic injury by activating Nrf2 and increasing HO-1 production [41]. The protective mechanisms are associated with the upregulation of HO-1, the activation of Nrf2, and the oxidation of 4-HHE. 4-HHE is the end-product of n-3 PUFAs by peroxidation and acts as an effective Nrf2 inducer [42]. Nrf2 acts as a transcription factor in regulating phase-2 enzymes expression. Under normal conditions, Kelch-like ECH-associated protein-1 (Keap1), the inhibitory protein of Nrf2, will bind to Nrf2 and lead Nrf2 to the proteasomal degradation process. Under oxidative stress, 4-HHE will react with the cysteine residues of Keap1 and dissociate Nrf2 from Keap1 [41]. Then Nrf2 will translocate into the nucleus, bind to antioxidant responsive element (ARE), and induce the expression of phase-2 enzymes [43]. Phase-2 enzymes like HO-1 mainly mediate the cytoprotection against oxidative stress, carcinogens, and toxicity. Cerebral ischemia/reperfusion injury will cause the elevated expression of antioxidative proteins and Keap1/Nrf2 system and increase the expression of Nrf2 and HO-1, which can inhibit the activation of microglia and the expression of proinflammatory cytokine [44]. The shortage of Nrf2 or HO-1 will sensitize animals to inflammation and injury induced by ischemic stroke. The neuroprotection against cerebral ischemic stroke mediated by DHA includes improving neuronal defense capacity and inhibiting cellular inflammatory mechanisms by increasing the expression of Nrf2 and HO-1 [45]. Although DHA itself is able to increase the expression of Nrf2 and HO-1 in glial cell cultures, it is not enough to induce the promotion of Nrf2 and HO-1 in vivo. Actually, the treatment with DHA after ischemic stroke only can provide a driving force for the promotion of Nrf2 and HO-1 [46].


The Role of Omega-3 Polyunsaturated Fatty Acids in Stroke.

Bu J, Dou Y, Tian X, Wang Z, Chen G - Oxid Med Cell Longev (2016)

The Nrf2/HO-1 signaling pathway induced by n-3 PUFAs.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4940554&req=5

fig2: The Nrf2/HO-1 signaling pathway induced by n-3 PUFAs.
Mentions: The dietary supplementation of n-3 PUFAs can decrease the volume of cerebral infarction partly by adjusting antioxidant enzymes activities and partly by working as an antioxidant directly [35]. n-3 PUFAs may act as an antioxidant in reducing cerebral lipid peroxides and play a role in regulating oxidative stress through the increase of oxidative burden and the improvement of antioxidative defense capacity [36]. The chronic administration and dietary supplementation of n-3 PUFAs can improve symptoms of cerebral I/R by increasing the antioxidative capacity, as well as reducing the induction of chaperon molecules and the stabilization of membrane integrity and lipid peroxidation [37]. The dietary supplementation of ALA is also found such that it can reduce the level of lipid peroxidation, as well as increasing the risk of spontaneous reperfusion [38]. The neuroprotective effects of n-3 PUFAs include not only inhibiting the oxidative stress but also enhancing the expression of nuclear factor E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) [39]. The Nrf2/HO-1 signaling pathway induced by n-3 PUFAs is shown in Figure 2. Nrf2/HO-1 signaling pathway is a crucial mechanism of n-3 PUFAs for protecting cells [40]. n-3 PUFAs reduce ischemic injury by activating Nrf2 and increasing HO-1 production [41]. The protective mechanisms are associated with the upregulation of HO-1, the activation of Nrf2, and the oxidation of 4-HHE. 4-HHE is the end-product of n-3 PUFAs by peroxidation and acts as an effective Nrf2 inducer [42]. Nrf2 acts as a transcription factor in regulating phase-2 enzymes expression. Under normal conditions, Kelch-like ECH-associated protein-1 (Keap1), the inhibitory protein of Nrf2, will bind to Nrf2 and lead Nrf2 to the proteasomal degradation process. Under oxidative stress, 4-HHE will react with the cysteine residues of Keap1 and dissociate Nrf2 from Keap1 [41]. Then Nrf2 will translocate into the nucleus, bind to antioxidant responsive element (ARE), and induce the expression of phase-2 enzymes [43]. Phase-2 enzymes like HO-1 mainly mediate the cytoprotection against oxidative stress, carcinogens, and toxicity. Cerebral ischemia/reperfusion injury will cause the elevated expression of antioxidative proteins and Keap1/Nrf2 system and increase the expression of Nrf2 and HO-1, which can inhibit the activation of microglia and the expression of proinflammatory cytokine [44]. The shortage of Nrf2 or HO-1 will sensitize animals to inflammation and injury induced by ischemic stroke. The neuroprotection against cerebral ischemic stroke mediated by DHA includes improving neuronal defense capacity and inhibiting cellular inflammatory mechanisms by increasing the expression of Nrf2 and HO-1 [45]. Although DHA itself is able to increase the expression of Nrf2 and HO-1 in glial cell cultures, it is not enough to induce the promotion of Nrf2 and HO-1 in vivo. Actually, the treatment with DHA after ischemic stroke only can provide a driving force for the promotion of Nrf2 and HO-1 [46].

Bottom Line: Evidence is accumulating that the dietary supplementation of fish oil exhibits beneficial effects on several diseases, such as cardiovascular diseases, metabolic diseases, and cancer.Omega-3 polyunsaturated fatty acids (n-3 PUFAs), the major component of fish oil, have been found against oxidative stress and inflammation in cardiovascular diseases.In this review, we will review the effects of n-3 PUFAs on stroke and mainly focus on the antioxidant and anti-inflammatory effects of n-3 PUFAs.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery & Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, 188 Shizi Street, Suzhou 215006, China.

ABSTRACT
Stroke is the third commonest cause of death following cardiovascular diseases and cancer. In particular, in recent years, the morbidity and mortality of stroke keep remarkable growing. However, stroke still captures people attention far less than cardiovascular diseases and cancer. Past studies have shown that oxidative stress and inflammation play crucial roles in the progress of cerebral injury induced by stroke. Evidence is accumulating that the dietary supplementation of fish oil exhibits beneficial effects on several diseases, such as cardiovascular diseases, metabolic diseases, and cancer. Omega-3 polyunsaturated fatty acids (n-3 PUFAs), the major component of fish oil, have been found against oxidative stress and inflammation in cardiovascular diseases. And the potential of n-3 PUFAs in stroke treatment is attracting more and more attention. In this review, we will review the effects of n-3 PUFAs on stroke and mainly focus on the antioxidant and anti-inflammatory effects of n-3 PUFAs.

No MeSH data available.


Related in: MedlinePlus