2017
DOI: 10.1038/srep43834
|View full text |Cite
|
Sign up to set email alerts
|

Abstract: This study aims to explore the effects of the TLR4 signaling pathway on the apoptosis of neuronal cells in rats with diabetes mellitus complicated with cerebral infarction (DMCI). A DMCI model was established with 40 Sprague Dawley rats, which were assigned into blank, sham, DM + middle cerebral artery occlusion (MCAO) and DM + MCAO + TAK242 groups. Superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were measured. A TUNEL assay was applied for detecting cell apoptosis, and Western blotting w… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
4
1

Citation Types

4
25
0

Year Published

2017
2017
2023
2023

Publication Types

Select...
9

Relationship

0
9

Authors

Journals

citations
Cited by 33 publications
(29 citation statements)
references
References 23 publications
4
25
0
Order By: Relevance
“…We also checked the anti-apoptotic effects of ALA. As expected, apoptotic markers were significantly elevated and anti-apoptotic marker expression was significantly reduced, which may be partly due to the upregulation of p-JNK, as mentioned previously [57]. Similarly, the upregulation of TLR4 and subsequent activation of astromicroglial cells may also contribute to the induction of apoptotic cell death and neurodegeneration [58]. Therefore, the inhibition of apoptotic cell death may be partly due to the inhibition of TLR4 and p-JNK.…”
Section: Discussionsupporting
confidence: 76%
“…We also checked the anti-apoptotic effects of ALA. As expected, apoptotic markers were significantly elevated and anti-apoptotic marker expression was significantly reduced, which may be partly due to the upregulation of p-JNK, as mentioned previously [57]. Similarly, the upregulation of TLR4 and subsequent activation of astromicroglial cells may also contribute to the induction of apoptotic cell death and neurodegeneration [58]. Therefore, the inhibition of apoptotic cell death may be partly due to the inhibition of TLR4 and p-JNK.…”
Section: Discussionsupporting
confidence: 76%
“…Inflammation is associated with apoptosis, which plays a key role in increased neuronal cell death after cerebral I/R injury. A recent experimental study in rats with diabetes and middle cerebral artery occlusion demonstrated that inhibition of the TLR4 signaling pathway significantly decreased neuronal cell apoptosis [ 26 ]. Caspase-3, which is a final and key enzyme of the intrinsic apoptotic cascade for neuronal apoptosis, was specifically involved [ 27 ].…”
Section: Discussionmentioning
confidence: 99%
“…These factors play vitals roles in regulating the innate and adaptive immune response, killing target cells, inducing apoptosis and inducing the production of acute phase reactive protein. Particularly, increased expression of these inflammatory factors have been proved in the serum of DM and DN patients (20). This finding suggest that TLR4 ligands can induce the production of rapid and strong inflammatory response by renal tubular epithelial cells and macrophages under hyperglycemia environment (19).…”
Section: Discussionmentioning
confidence: 83%
“…This finding suggest that TLR4 ligands can induce the production of rapid and strong inflammatory response by renal tubular epithelial cells and macrophages under hyperglycemia environment (19). In addition, it demonstrates that renal cell itself can be involved in the inflammatory response of DN through activating TLR4 (20). Zhang et al indicated that UA alleviates early brain injury by suppressing TLR4-mediated inflammatory pathway (12).…”
Section: Discussionmentioning
confidence: 95%