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Nicorandil attenuates neuronal mitochondrial dysfunction and oxidative stress associated with murine model of vascular calcification.

Abstract Evidences suggest that the presence of chronic kidney disease (CKD) is associated with cerebrovascular diseases related cognitive decline in dialysis patients. As mitochondrial dysfunction is implicated in neurodegenerative disorders, we hypothesized that changes in brain mitochondria occur due to vascular calcification induced by renal failure and the opening of the mitochondrial potassium channel using nicorandil may prevent its dysfunction. Brain tissues from rats with vascular calcification were studied. Nicorandil (7.5 mg/kg b.wt.) was given either concomitantly or after the induction of calcification. The brain tissues were evaluated for antioxidant capacity, mitochondrial enzymes and oxidative phosphorylation efficiency along with the progression of calcification. The results suggested that renal failure, elevated the calcium, phosphorus product in the brain. The brain cytoplasm and mitochondrial fractions showed an elevated TBARS and a corresponding decline in the antioxidant enzymes, indicating a sev ere oxidative stress. The elevated brain mitochondrial enzymes like NADH dehydrogenase, and succinate dehydrogenase in the disease control groups, reversed to the near control level after nicorandil treatment. We observed that nicorandil was more effective when given after calcification. It reduced the biochemical alterations associated with calcium and phosphorous toxicity in the brain, by preserving mitochondria, the key target for treating neurodegenerative diseases.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title acta neurobiologiae experimentalis
Publication Year Start




PMID- 28379216
OWN - NLM
STAT- MEDLINE
DA  - 20170405
DCOM- 20170414
LR  - 20170414
IS  - 1689-0035 (Electronic)
IS  - 0065-1400 (Linking)
VI  - 77
IP  - 1
DP  - 2017
TI  - Nicorandil attenuates neuronal mitochondrial dysfunction and oxidative stress
      associated with murine model of vascular calcification.
PG  - 57-67
AB  - Evidences suggest that the presence of chronic kidney disease (CKD) is associated
      with cerebrovascular diseases related cognitive decline in dialysis patients. As 
      mitochondrial dysfunction is implicated in neurodegenerative disorders, we
      hypothesized that changes in brain mitochondria occur due to vascular
      calcification induced by renal failure and the opening of the mitochondrial
      potassium channel using nicorandil may prevent its dysfunction. Brain tissues
      from rats with vascular calcification were studied. Nicorandil (7.5 mg/kg b.wt.) 
      was given either concomitantly or after the induction of calcification. The brain
      tissues were evaluated for antioxidant capacity, mitochondrial enzymes and
      oxidative phosphorylation efficiency along with the progression of calcification.
      The results suggested that renal failure, elevated the calcium, phosphorus
      product in the brain. The brain cytoplasm and mitochondrial fractions showed an
      elevated TBARS and a corresponding decline in the antioxidant enzymes, indicating
      a sev ere oxidative stress. The elevated brain mitochondrial enzymes like NADH
      dehydrogenase, and succinate dehydrogenase in the disease control groups,
      reversed to the near control level after nicorandil treatment. We observed that
      nicorandil was more effective when given after calcification. It reduced the
      biochemical alterations associated with calcium and phosphorous toxicity in the
      brain, by preserving mitochondria, the key target for treating neurodegenerative 
      diseases.
FAU - Ravindran, Sriram
AU  - Ravindran S
AD  - Vascular Biology Lab, SASTRA University, Thanjavur, India.
FAU - Swaminathan, Krithika
AU  - Swaminathan K
AD  - School of Chemical and Biotechnology, SASTRA University, Thanjavur, India.
FAU - Ramesh, Abhinaya
AU  - Ramesh A
AD  - School of Chemical and Biotechnology, SASTRA University, Thanjavur, India.
FAU - Kurian, Gino A
AU  - Kurian GA
AD  - Vascular Biology Lab, SASTRA University, Thanjavur, India,
      [email protected]
LA  - eng
PT  - Journal Article
PL  - Poland
TA  - Acta Neurobiol Exp (Wars)
JT  - Acta neurobiologiae experimentalis
JID - 1246675
RN  - 0 (Free Radical Scavengers)
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (Thiobarbituric Acid Reactive Substances)
RN  - 12001-76-2 (Vitamin B Complex)
RN  - 260456HAM0 (Nicorandil)
RN  - 27YLU75U4W (Phosphorus)
RN  - EC 1.11.1.6 (Catalase)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Aorta/pathology
MH  - Calcium/metabolism
MH  - Catalase/metabolism
MH  - Drug Administration Schedule
MH  - Free Radical Scavengers/metabolism
MH  - Histocompatibility Antigens Class I/metabolism
MH  - Kidney Function Tests
MH  - Lipid Peroxidation/drug effects
MH  - Mitochondria/*drug effects/metabolism/ultrastructure
MH  - Mitochondrial Diseases/*drug therapy/etiology
MH  - Nicorandil/pharmacology/*therapeutic use
MH  - Oxidative Stress/*drug effects
MH  - Phosphorus/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Renal Insufficiency, Chronic/complications/diagnosis
MH  - Thiobarbituric Acid Reactive Substances/metabolism
MH  - Vascular Calcification/etiology/*prevention & control
MH  - Vitamin B Complex/pharmacology/*therapeutic use
EDAT- 2017/04/06 06:00
MHDA- 2017/04/15 06:00
CRDT- 2017/04/06 06:00
AID - 7705 [pii]
PST - ppublish
SO  - Acta Neurobiol Exp (Wars). 2017;77(1):57-67.

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