Studies have shown that C1q/tumor necrosis factor-related protein-6 (CTRP6) can alleviate renal ischemia/reperfusion injury in mice. However, its role in the brain remains poorly understood. To investigate the role of...Studies have shown that C1q/tumor necrosis factor-related protein-6 (CTRP6) can alleviate renal ischemia/reperfusion injury in mice. However, its role in the brain remains poorly understood. To investigate the role of CTRP6 in cerebral ischemia/reperfusion injury associated with diabetes mellitus, a diabetes mellitus mouse model of cerebral ischemia/reperfusion injury was established by occlusion of the middle cerebral artery. To overexpress CTRP6 in the brain, an adeno-associated virus carrying CTRP6 was injected into the lateral ventricle. The result was that oxygen injury and inflammation in brain tissue were clearly attenuated, and the number of neurons was greatly reduced. In vitro experiments showed that CTRP6 knockout exacerbated oxidative damage, inflammatory reaction, and apoptosis in cerebral cortical neurons in high glucose hypoxia-simulated diabetic cerebral ischemia/reperfusion injury. CTRP6 overexpression enhanced the sirtuin-1 signaling pathway in diabetic brains after ischemia/reperfusion injury. To investigate the mechanism underlying these effects, we examined mice with depletion of brain tissue-specific sirtuin-1. CTRP6-like protection was achieved by activating the sirtuin-1 signaling pathway. Taken together, these results indicate that CTRP6 likely attenuates cerebral ischemia/reperfusion injury through activation of the sirtuin-1 signaling pathway.展开更多
The present study established a rabbit model of global cerebral ischemia using the 'six-vessel' method,which was reperfused after 30 minutes of ischemia.Rabbits received intravenous injection of propofol at 5 ...The present study established a rabbit model of global cerebral ischemia using the 'six-vessel' method,which was reperfused after 30 minutes of ischemia.Rabbits received intravenous injection of propofol at 5 mg/kg prior to ischemia and 20 mg/kg per hour after ischemia until samples were prepared.Results revealed that propofol inhibited serum interleukin-8,endothelin-1 and malondialdehyde increases and promoted plasma superoxide dismutase activity after cerebral ischemia/reperfusion.In addition,cerebral cortex edema was attenuated with little neuronal nuclear degeneration and pyknosis with propofol treatment.The cross-sectional area of neuronal nuclei was,however,increased following propofol treatment.These findings suggested that propofol could improve anti-oxidant activity and inhibit synthesis of inflammatory factors to exert a protective effect on cerebral ischemia/reperfusion injury.展开更多
The present study established global brain ischemia using the four-vessel occlusion method.Following three rounds of reperfusion for 30 seconds,and occlusion for 10 seconds,followed by reperfusion for 48 hours,infarct...The present study established global brain ischemia using the four-vessel occlusion method.Following three rounds of reperfusion for 30 seconds,and occlusion for 10 seconds,followed by reperfusion for 48 hours,infarct area,the number of TUNEL-positive cells and Bcl-2 expression were significantly reduced.However,glycogen synthase kinase-3β activity,cortical Bax and caspase-3 expression significantly increased,similar to results following ischemic postconditioning.Our results indicated that ischemic postconditioning may enhance glycogen synthase kinase-3β activity,a downstream molecule of the phosphatase and tensin homolog deleted on chromosome 10/phosphatidylinositol 3-kinase/protein kinase B signaling pathway,which reduces caspase-3 expression to protect the brain against ischemic injury.展开更多
Natural alleles controlling multiple disease resistances (MDR) are valuable for crop breeding. However, only one MDR gene have been cloned in maize, and molecular mechanisms of MDR are not clear. By map-based cloning,...Natural alleles controlling multiple disease resistances (MDR) are valuable for crop breeding. However, only one MDR gene have been cloned in maize, and molecular mechanisms of MDR are not clear. By map-based cloning, we have cloned a teosinte-derived allele of a resistance gene, Mexicana lesion mimic 1 (ZmMM1), which has a lesion mimic phenotype and confers resistance to northern leaf blight (NLB), gray leaf spot (GLS) and southern corn rust (SCR). Strong MDR conferred by the teosinte allele is linked with the polymorphisms in the 3' untranslated region of the ZmMM1 gene that cause increased accumulation of ZmMM1 protein. ZmMM1 acts as a transcription repressor and negatively regulates transcription of specific target genes including ZmMM1-target gene 3 (ZmMT3), which functions as a negative regulator of plant immunity and associated cell death. The successful isolation of the ZmMM1 resistance gene will help not only in developing broad-spectrum and durable disease resistance but also in understanding the molecular mechanisms underlying MDR.展开更多
基金supported by the National Natural Science Foundation of China,Nos.82102295(to WG),82071339(to LG),82001119(to JH),and 81901994(to BZ).
文摘Studies have shown that C1q/tumor necrosis factor-related protein-6 (CTRP6) can alleviate renal ischemia/reperfusion injury in mice. However, its role in the brain remains poorly understood. To investigate the role of CTRP6 in cerebral ischemia/reperfusion injury associated with diabetes mellitus, a diabetes mellitus mouse model of cerebral ischemia/reperfusion injury was established by occlusion of the middle cerebral artery. To overexpress CTRP6 in the brain, an adeno-associated virus carrying CTRP6 was injected into the lateral ventricle. The result was that oxygen injury and inflammation in brain tissue were clearly attenuated, and the number of neurons was greatly reduced. In vitro experiments showed that CTRP6 knockout exacerbated oxidative damage, inflammatory reaction, and apoptosis in cerebral cortical neurons in high glucose hypoxia-simulated diabetic cerebral ischemia/reperfusion injury. CTRP6 overexpression enhanced the sirtuin-1 signaling pathway in diabetic brains after ischemia/reperfusion injury. To investigate the mechanism underlying these effects, we examined mice with depletion of brain tissue-specific sirtuin-1. CTRP6-like protection was achieved by activating the sirtuin-1 signaling pathway. Taken together, these results indicate that CTRP6 likely attenuates cerebral ischemia/reperfusion injury through activation of the sirtuin-1 signaling pathway.
文摘The present study established a rabbit model of global cerebral ischemia using the 'six-vessel' method,which was reperfused after 30 minutes of ischemia.Rabbits received intravenous injection of propofol at 5 mg/kg prior to ischemia and 20 mg/kg per hour after ischemia until samples were prepared.Results revealed that propofol inhibited serum interleukin-8,endothelin-1 and malondialdehyde increases and promoted plasma superoxide dismutase activity after cerebral ischemia/reperfusion.In addition,cerebral cortex edema was attenuated with little neuronal nuclear degeneration and pyknosis with propofol treatment.The cross-sectional area of neuronal nuclei was,however,increased following propofol treatment.These findings suggested that propofol could improve anti-oxidant activity and inhibit synthesis of inflammatory factors to exert a protective effect on cerebral ischemia/reperfusion injury.
基金sponsored by the National Natural Science Foundation of China,No.81170768
文摘The present study established global brain ischemia using the four-vessel occlusion method.Following three rounds of reperfusion for 30 seconds,and occlusion for 10 seconds,followed by reperfusion for 48 hours,infarct area,the number of TUNEL-positive cells and Bcl-2 expression were significantly reduced.However,glycogen synthase kinase-3β activity,cortical Bax and caspase-3 expression significantly increased,similar to results following ischemic postconditioning.Our results indicated that ischemic postconditioning may enhance glycogen synthase kinase-3β activity,a downstream molecule of the phosphatase and tensin homolog deleted on chromosome 10/phosphatidylinositol 3-kinase/protein kinase B signaling pathway,which reduces caspase-3 expression to protect the brain against ischemic injury.
基金This work was supported by the National Key Research and Development Program of China(2016YFD0101002)the National Natural Science Foundation of China(31571676,32072007,and 31761143008)+4 种基金the Ministry of Science and Technology of the People's Republic of China(2015BAD02B01)the Fundamental Research Funds for the Central Universities(2014PY054 and 2662015PY185)the University Student Research Fund(2016090)the Innovation Training Plan of University Student Fund(201510504023)the Higher Education Discipline Innovation Project(B20051).
文摘Natural alleles controlling multiple disease resistances (MDR) are valuable for crop breeding. However, only one MDR gene have been cloned in maize, and molecular mechanisms of MDR are not clear. By map-based cloning, we have cloned a teosinte-derived allele of a resistance gene, Mexicana lesion mimic 1 (ZmMM1), which has a lesion mimic phenotype and confers resistance to northern leaf blight (NLB), gray leaf spot (GLS) and southern corn rust (SCR). Strong MDR conferred by the teosinte allele is linked with the polymorphisms in the 3' untranslated region of the ZmMM1 gene that cause increased accumulation of ZmMM1 protein. ZmMM1 acts as a transcription repressor and negatively regulates transcription of specific target genes including ZmMM1-target gene 3 (ZmMT3), which functions as a negative regulator of plant immunity and associated cell death. The successful isolation of the ZmMM1 resistance gene will help not only in developing broad-spectrum and durable disease resistance but also in understanding the molecular mechanisms underlying MDR.
