PMID- 30551358
OWN - NLM
STAT- MEDLINE
DCOM- 20190328
LR  - 20190328
IS  - 1950-6007 (Electronic)
IS  - 0753-3322 (Linking)
VI  - 109
DP  - 2019 Jan
TI  - Mechanistic role of cAMP and hepatocyte growth factor signaling in 
      thioacetamide-induced nephrotoxicity: Unraveling the role of platelet rich 
      plasma.
PG  - 1078-1084
LID - S0753-3322(18)36589-2 [pii]
LID - 10.1016/j.biopha.2018.10.121 [doi]
AB  - Chronic kidney diseases occur as result of exposure to wide range of deleterious 
      agents as environmental pollutants, toxins and drug. Currently, there is no 
      effective protective therapy against renal damage, fibrosis and its sequel of end 
      stage renal disease. Platelet-rich plasma (PRP) has a progressively gained 
      consideration in wound healing, repair/regeneration of damaged tissues and 
      conservation of organ function. However, its impact on thioacetamide (TAA) 
      induced chronic renal damage has not been elucidated yet. So, the present study 
      was carried out to evaluate the possible protective and regenerative effect of 
      PRP against TAA induced renal damage and their potential underlying mechanism. 
      PRP treatment improved redox state, renal function disturbed histologicl 
      features; decreased monocyte chemo-attractant protein-1 (MCP-1) level; increased 
      Peroxisome proliferator-activated receptor gamma co-activator-1alpha (PGC-1alpha) marker 
      of mitochondrial biogenesis and metabolism; cyclic adenosine monophosphate 
      (cAMP); hepatocyte growth factor (HGF) and autophagy protein beclin-1 level. In 
      addition, PRP treatment decreased apoptosis and fibrosis as evidenced by 
      decreased active caspase3 and alpha-SMA expression and immunoreactivity, 
      respectively. In conclusion, PRP could potentially protect against TTA-induced 
      chronic kidney damage by alleviating oxidative stress, improving, mitochondrial 
      biogenesis, autophagy, disruption of the inflammatory, apoptotic and fibrotic 
      response induced by TTA.
CI  - Copyright (c) 2018 Elsevier Masson SAS. All rights reserved.
FAU - Keshk, Walaa Arafa
AU  - Keshk WA
AD  - Medical Biochemistry Department, Faculty of Medicine, Tanta University, El-Geish 
      Street, Tanta, El-Gharbia, Egypt. Electronic address: walaaarafaa@gmail.com.
FAU - Zahran, Samer Mahmoud
AU  - Zahran SM
AD  - Biochemistry Department, Faculty of Pharmacy and Drug Manufacturing, Pharos 
      University, Alexandria, Egypt.
LA  - eng
PT  - Journal Article
DEP - 20181106
PL  - France
TA  - Biomed Pharmacother
JT  - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
JID - 8213295
RN  - 0 (Beclin-1)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha)
RN  - 0 (Transcription Factors)
RN  - 075T165X8M (Thioacetamide)
RN  - 67256-21-7 (Hepatocyte Growth Factor)
RN  - E0399OZS9N (Cyclic AMP)
SB  - IM
MH  - Animals
MH  - Apoptosis/physiology
MH  - Autophagy/physiology
MH  - Beclin-1/metabolism
MH  - Chemokine CCL2/metabolism
MH  - Cyclic AMP/*metabolism
MH  - Hepatocyte Growth Factor/*metabolism
MH  - Male
MH  - Mitochondria/metabolism
MH  - Oxidation-Reduction
MH  - Oxidative Stress/physiology
MH  - Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism
MH  - Platelet-Rich Plasma/*metabolism
MH  - Rats
MH  - Renal Insufficiency, Chronic/*chemically induced/*metabolism
MH  - Signal Transduction/*physiology
MH  - Thioacetamide/*pharmacology
MH  - Transcription Factors/metabolism
OTO - NOTNLM
OT  - Beclin-1
OT  - Cyclic adenosine monophosphate
OT  - Hepatocyte growth factor (HGF)
OT  - Monocyte chemo-attractant protein-1
OT  - Peroxisome proliferator-activated receptor gamma co-activator-1??
OT  - Platelet rich plasma
OT  - Thioacetamide
EDAT- 2018/12/16 06:00
MHDA- 2019/03/29 06:00
CRDT- 2018/12/16 06:00
PHST- 2018/09/14 00:00 [received]
PHST- 2018/10/16 00:00 [revised]
PHST- 2018/10/20 00:00 [accepted]
PHST- 2018/12/16 06:00 [entrez]
PHST- 2018/12/16 06:00 [pubmed]
PHST- 2019/03/29 06:00 [medline]
AID - S0753-3322(18)36589-2 [pii]
AID - 10.1016/j.biopha.2018.10.121 [doi]
PST - ppublish
SO  - Biomed Pharmacother. 2019 Jan;109:1078-1084. doi: 10.1016/j.biopha.2018.10.121. 
      Epub 2018 Nov 6.