PMID- 30919248 OWN - NLM STAT- MEDLINE DCOM- 20190604 LR - 20220218 IS - 1559-1166 (Electronic) IS - 0895-8696 (Linking) VI - 68 IP - 2 DP - 2019 Jun TI - Apparent Correlations Between AMPK Expression and Brain Inflammatory Response and Neurological Function Factors in Rats with Chronic Renal Failure. PG - 204-213 LID - 10.1007/s12031-019-01299-8 [doi] AB - To explore the correlations between AMP-activated protein kinase (AMPK) expression and brain inflammatory response and neurological function factors in rats with chronic renal failure. Chronic renal failure models in rats were established, and the healthy control group (normal group) was set. Chronic renal failure model rats were divided into model group (without any treatment), control group (intraperitoneal injection of normal saline), A-769662 group (intraperitoneal injection of AMPK specific activator), and compound C group (intraperitoneal injection of AMPK specific inhibitor). The results of HE staining showed renal tissue enlargement, and significant pathological changes. Compared with the normal group, AMPK level in peripheral blood and AMPK mRNA and protein expressions in brain tissue were significantly reduced, and AMPK pathway activation was significantly inhibited in other groups. Compared with the model group, rats in the A-769662 group had significantly decreased serum creatinine (Scr) and blood urea nitrogen (BUN) levels and gamma-aminobutyric acid (gamma-GABA) content, significantly increased brain-derived neurotrophic factor (BDNF) positive expressions and 5-hydroxytryptamine (5-HT) content, and decreased interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), and intercellular adhesion molecule 1 (ICAM-1) expressions (all P < 0.05), while it was just the opposite in compound C group (all P < 0.05). There is an apparent correlation between AMPK expression and brain inflammatory response in chronic renal failure rats. AMPK is expected to be an important pathway in the treatment of uremic encephalopathy. FAU - Yang, Li AU - Yang L AD - Department of Nephrology, Nanfang Hospital, Southern Medical University, No. 1838 North Guangzhou Avenue, Guangzhou, 510515, Guangdong Province, China. FAU - Gong, Ni-Rong AU - Gong NR AD - Department of Nephrology, Nanfang Hospital, Southern Medical University, No. 1838 North Guangzhou Avenue, Guangzhou, 510515, Guangdong Province, China. FAU - Zhang, Qin AU - Zhang Q AD - Department of Nephrology, Nanfang Hospital, Southern Medical University, No. 1838 North Guangzhou Avenue, Guangzhou, 510515, Guangdong Province, China. FAU - Ma, Ya-Bin AU - Ma YB AD - Department of Neurosurgery, The First Affiliated Hospital of Guangdong Pharmaceutical University, No. 19 Nonglin Xia Road, Yuexiu District, Guangzhou, 510080, Guangdong Province, China. FAU - Zhou, Hui AU - Zhou H AUID- ORCID: 0000-0003-4697-4508 AD - Department of Neurosurgery, The First Affiliated Hospital of Guangdong Pharmaceutical University, No. 19 Nonglin Xia Road, Yuexiu District, Guangzhou, 510080, Guangdong Province, China. zhouhui291@163.com. LA - eng GR - B2015106/Medical Scientific Research Foundation of Guangdong Province, China/ GR - 81470995/National Natural Science Foundation of China/ PT - Journal Article DEP - 20190327 PL - United States TA - J Mol Neurosci JT - Journal of molecular neuroscience : MN JID - 9002991 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Interleukin-1) RN - 0 (Tumor Necrosis Factor-alpha) RN - 126547-89-5 (Intercellular Adhesion Molecule-1) RN - EC 2.7.- (Protein Kinases) RN - EC 2.7.11.3 (AMP-Activated Protein Kinase Kinases) SB - IM MH - AMP-Activated Protein Kinase Kinases MH - Animals MH - Brain/*metabolism MH - Brain-Derived Neurotrophic Factor/genetics/*metabolism MH - Intercellular Adhesion Molecule-1/genetics/metabolism MH - Interleukin-1/genetics/*metabolism MH - Kidney Failure, Chronic/*metabolism MH - Male MH - Protein Kinases/*genetics/metabolism MH - Rats MH - Rats, Sprague-Dawley MH - Tumor Necrosis Factor-alpha/genetics/*metabolism OTO - NOTNLM OT - AMPK pathway OT - Brain inflammation OT - Chronic renal failure OT - Neurological function factor EDAT- 2019/03/29 06:00 MHDA- 2019/06/05 06:00 CRDT- 2019/03/29 06:00 PHST- 2019/01/22 00:00 [received] PHST- 2019/03/12 00:00 [accepted] PHST- 2019/03/29 06:00 [pubmed] PHST- 2019/06/05 06:00 [medline] PHST- 2019/03/29 06:00 [entrez] AID - 10.1007/s12031-019-01299-8 [pii] AID - 10.1007/s12031-019-01299-8 [doi] PST - ppublish SO - J Mol Neurosci. 2019 Jun;68(2):204-213. doi: 10.1007/s12031-019-01299-8. Epub 2019 Mar 27.