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Published on: August 9, 2013
Complement Component C3 Promotes Cerebral Ischemia/Reperfusion Injury Mediated by TLR2/NFκB Activation in Diabetic
Zheng Lin1, Haoran Lin1, Wenlu Li1
1Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310009, China.
Insights
Complement component C3 (C3) exacerbates diabetic stroke by activating the TLR2/NFκB pathway. C3 deficiency protects against cerebral ischemia/reperfusion injury in diabetic mice, suggesting a therapeutic target.
Area of Science:
- Immunology
- Neuroscience
- Pathology
Background:
- Complement component C3 (C3) is implicated in inflammation but its role in diabetic stroke pathogenesis is unclear.
- Cerebral ischemia/reperfusion (I/R) injury is a significant complication in diabetes.
Purpose of the Study:
- To investigate the role of complement C3 in cerebral I/R injury in a diabetic mouse model.
- To elucidate the underlying molecular pathway involving C3 in diabetic stroke.
Main Methods:
- Transient middle cerebral artery occlusion (tMCAO) model in streptozotocin-induced diabetic mice.
- Assessment of cerebral infarct volume and neurological function.
- Measurement of complement C3, TLR2, and NFκB activation using ELISA and Western blotting.
Main Results:
- Complement C3 expression was significantly increased in diabetic mice following cerebral I/R injury.
- C3 deficiency attenuated cerebral I/R injury and neurological deficits.
- C3 activation promoted TLR2/NFκB activation, which was reversed by TLR2 silencing.
Conclusions:
- Complement C3 significantly contributes to cerebral I/R injury in diabetic mice.
- The C3/TLR2/NFκB pathway mediates diabetic stroke pathogenesis.
- Targeting the C3/TLR2/NFκB pathway offers a potential therapeutic strategy for diabetic stroke.
Abstract:
Complement component C3 (C3), a key factor in the complement system, is heavily involved in various inflammation-associated diseases. However, it remains obscure for its role in the pathogenesis of cerebral ischemia/reperfusion (I/R) injury in diabetes. A transient middle cerebral artery occlusion (tMCAO) model was used for cerebral I/R injury in streptozotocin-induced diabetic mice. Cerebral infarct volume and neurological function were measured at different times of reperfusion. Complement C3 was measured by ELISA and western blotting. It was observed that complement C3 expression was increased in cerebral I/R injury of diabetic mice, whereas complement C3 deficiency abrogated the activation and injury. Furthermore, activating complement C3 promotes TLR2/NFκB activation after I/R injury in diabetic mice, which is inhibited by of the silencing of TLR2. Taken together, our data demonstrate that complement C3 promotes cerebral I/R injury via the TLR2/NFκB pathway in diabetic mice, and regulating the complement C3/TLR2/NFκB pathway may be a novel target for therapeutic intervention in diabetic stroke.
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