To examine the effects of Cerebrolysin on the treatment of diabetic peripheral neuropathy, we first established a mouse model of type 2 diabetes mellitus by administering a high-glucose, high-fat diet and a single int...To examine the effects of Cerebrolysin on the treatment of diabetic peripheral neuropathy, we first established a mouse model of type 2 diabetes mellitus by administering a high-glucose, high-fat diet and a single intraperitoneal injection of streptozotocin. Mice defined as diabetic in this model were then treated with 1.80, 5.39 or 8.98 m L/kg of Cerebrolysin via intraperitoneal injections for 10 consecutive days. Our results demonstrated that the number, diameter and area of myelinated nerve fibers increased in the sciatic nerves of these mice after administration of Cerebrolysin. The results of several behavioral tests showed that Cerebrolysin dose-dependently increased the slope angle in the inclined plane test（indicating an improved ability to maintain body position）, prolonged tail-flick latency and foot-licking time（indicating enhanced sensitivity to thermal and chemical pain, respectively, and reduced pain thresholds）, and increased an index of sciatic nerve function in diabetic mice compared with those behavioral results in untreated diabetic mice. Taken together, the anatomical and functional results suggest that Cerebrolysin ameliorated peripheral neuropathy in a mouse model of type 2 diabetes mellitus.展开更多
Hengel et al recently reported that bi-allelic loss-of-function mutations in UDP-Glucose 6-Dehydrogenase(UGDH)caused a severe epileptic encephalopathy syndrome-Jamuar syndrome(OMIM#618792).1 The functional studies par...Hengel et al recently reported that bi-allelic loss-of-function mutations in UDP-Glucose 6-Dehydrogenase(UGDH)caused a severe epileptic encephalopathy syndrome-Jamuar syndrome(OMIM#618792).1 The functional studies partially recapitulated the clinical phenotypes in the patient-derived cerebral organoid.A reduced number of proliferating neuronal progenitors in cerebral organoids was shown,which is a critical mechanism in congenital microcephaly(CM)whose patients were born with an occipitofrontal circumference(OCF)more than 2 standard deviations below average for age and sex.However,none of the reported patients in the article presented the phenotype as CM.展开更多
文摘To examine the effects of Cerebrolysin on the treatment of diabetic peripheral neuropathy, we first established a mouse model of type 2 diabetes mellitus by administering a high-glucose, high-fat diet and a single intraperitoneal injection of streptozotocin. Mice defined as diabetic in this model were then treated with 1.80, 5.39 or 8.98 m L/kg of Cerebrolysin via intraperitoneal injections for 10 consecutive days. Our results demonstrated that the number, diameter and area of myelinated nerve fibers increased in the sciatic nerves of these mice after administration of Cerebrolysin. The results of several behavioral tests showed that Cerebrolysin dose-dependently increased the slope angle in the inclined plane test（indicating an improved ability to maintain body position）, prolonged tail-flick latency and foot-licking time（indicating enhanced sensitivity to thermal and chemical pain, respectively, and reduced pain thresholds）, and increased an index of sciatic nerve function in diabetic mice compared with those behavioral results in untreated diabetic mice. Taken together, the anatomical and functional results suggest that Cerebrolysin ameliorated peripheral neuropathy in a mouse model of type 2 diabetes mellitus.
基金supported by the Natural Science Foundation of Hunan Province,China(No.2021JJ40280)the National Key Research and Development Program of China(No.2021YFC1005300)+4 种基金the Major Scientific and Technological Projects for Collaborative Prevention and Control of Birth Defects in Hunan Province,China(No.2019SK1010,2019SK1014)the National Key R&D Program of China(No.2019YFC1005100)the Hunan Provincial Science and Technology Department(China)(No.2018SK2064)the Joint Construction Project of Henan Medical Science and Technology Project(China)(No.LHGJ20200618,2018020633)the Henan Engineering Research Center of Childhood Neurodevelopment Open Project(China)(No.SG201907).
文摘Hengel et al recently reported that bi-allelic loss-of-function mutations in UDP-Glucose 6-Dehydrogenase(UGDH)caused a severe epileptic encephalopathy syndrome-Jamuar syndrome(OMIM#618792).1 The functional studies partially recapitulated the clinical phenotypes in the patient-derived cerebral organoid.A reduced number of proliferating neuronal progenitors in cerebral organoids was shown,which is a critical mechanism in congenital microcephaly(CM)whose patients were born with an occipitofrontal circumference(OCF)more than 2 standard deviations below average for age and sex.However,none of the reported patients in the article presented the phenotype as CM.
