The protective effect of metformin on mitochondrial dysfunction and endoplasmic reticulum stress in diabetic mice brain.
Diabetes is a metabolic disorder associated with mitochondrial (mt) dysfunction and oxidative stress. The molecular mechanisms involved in diabetes-associated neurological complications remain elusive. This study aims to investigate the protective effect of metformin (MF) on regulatory networks and integrated stress responses in brain tissue of Streptozotocin (STZ)-induced diabetic mice. STZ-induced diabetic mice were treated with MF (20 mg/kg BW), and whole brain tissue was harvested for further analysis. Protein carbonylation was measured as a marker of neuronal oxidative stress. Protein expression of mt chaperones, maintenance proteins, and regulators of the unfolded protein response (UPR) were measured by Western blot. Transcript levels of antioxidant enzyme GSTA4; mt biogenesis markers, ER stress regulators, and miR-132 and miR-148a were analysed using qPCR.
The results showed that MF efficiently reduced protein carbonylation and oxidation. Mt function was improved by MF-treatment through upregulation of chaperone proteins (HSP60, HSP70 and LonP1). MF elicits the UPR to attenuate ER stress through a miR-132 repression mechanism. Additionally, MF was found to elevate deacetylases- Sirt1, Sirt3; and mt biogenesis marker PGC-1α through miR-148a repression. This is the first study to demonstrate the epigenetic regulation of mt maintenance by MF in diabetic C57BL/6 mouse whole brain tissue. We thus conclude that MF, beyond its anti-hyperglycaemic role, mediates neuroprotection through epigenomic and integrated stress responses in diabetic mice.
Immunogen information: Synthesized peptide derived from the C-terminal region of human Neuronal PAS1 at AA range: 420-500
Applications tips:
Description: A polyclonal antibody for detection of Neuronal PAS1 from Human. This Neuronal PAS1 antibody is for WB, ELISA. It is affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogenand is unconjugated. The antibody is produced in rabbit by using as an immunogen synthesized peptide derived from the C-terminal region of human Neuronal PAS1 at AA range: 420-500
Immunogen information: Synthesized peptide derived from the C-terminal region of human Neuronal PAS1 at AA range: 420-500
Applications tips:
Description: A polyclonal antibody for detection of Neuronal PAS1 from Human. This Neuronal PAS1 antibody is for WB, ELISA. It is affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogenand is unconjugated. The antibody is produced in rabbit by using as an immunogen synthesized peptide derived from the C-terminal region of human Neuronal PAS1 at AA range: 420-500
Immunogen information: Synthesized peptide derived from the C-terminal region of human Neuronal PAS1 at AA range: 420-500
Applications tips:
Description: A polyclonal antibody for detection of Neuronal PAS1 from Human. This Neuronal PAS1 antibody is for WB, ELISA. It is affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogenand is unconjugated. The antibody is produced in rabbit by using as an immunogen synthesized peptide derived from the C-terminal region of human Neuronal PAS1 at AA range: 420-500
Abnormal amygdala subregional-sensorimotor connectivity correlates with positive symptom in schizophrenia.
Altered resting-state functional connectivity (rsFC) of the amygdala has been demonstrated to be implicated in schizophrenia neuronal pathophysiology. However, whether rsFC of amygdala subregions is differentially affected in schizophrenia remains unclear.
This study compared the functional networks of each amygdala subdivision between healthy controls (HC) and patients with first-episode schizophrenia (FES). In total, 47 HC and 78 patients with FES underwent resting-state functional magnetic resonance imaging. The amygdala was divided into the following three subregions using the Juelich histological atlas: basolateral amygdala (BLA), centromedial amygdala (CMA), and superficial amygdala (SFA). The rsFC of the three amygdala subdivisions was computed and compared between the two groups. Significantly increased rsFC of the right CMA with the right postcentral gyrus and decreased rsFC of the right BLA with the left precentral gyrus were observed in the FES group compared with the HC group. Notably, the right BLA-left precentral gyrus connectivity was negatively correlated with positive symptoms and conceptual disorganization in patients with FES.
In conclusion, this study found that patients with FES had abnormal functional connectivity in the amygdala subregions, and the altered rsFC was associated with positive symptoms. The present findings demonstrate the disruptive rsFC patterns of amygdala subregional-sensorimotor networks in FES and may provide new insights into the neuronal pathophysiology of FES. Time courses of HMGB1 and other inflammatory markers after generalized convulsive seizures.
Neuroinflammation and disruption of blood brain barrier (BBB) are important players in epileptogenesis, ictogenesis and pharmacoresistance.
In this context, we investigated blood levels of HMGB1 and other inflammatory and BBB markers after generalized and focal to bilateral tonic-clonic seizures in serum, summarized under the term generalized convulsive seizures (GCS).We included consenting adults who were admitted to the epilepsy monitoring unit. Blood samples were drawn at baseline and immediately after a GCS as well as after 2, 6 and 24 h. We measu
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