Wild type mice were given tunicamycin (TM; 0.5 mg/kg I.P) for three days with or without vorinostat (vor; 50 mg/kg/day) or 4-phenylbutyrate (PBA; 1 g/kg/day).

<p>(A) Kidneys were PAS stained to examine structural damage in the pars recta. Damage is indicated with arrows. (B) Kidney injury scores demonstrate TM caused significant damage in the pars recta, with TM+vor-treated mice having similar levels of damage. (C) Serum creatinine levels were incre...

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التفاصيل البيبلوغرافية
المؤلف الرئيسي:	Rachel E. Carlisle (11772751) (author)
مؤلفون آخرون:	Salwa Farooqi (11772754) (author), Ming Chan Zhang (11772757) (author), Sarah Liu (6569135) (author), Chao Lu (4374) (author), Andy Phan (11772760) (author), Elise Brimble (506600) (author), Jeffrey G. Dickhout (11772763) (author)
منشور في:	2021
الموضوعات:	Biochemistry Microbiology Cell Biology Molecular Biology Pharmacology Biotechnology Marine Biology Biological Sciences not elsewhere classified Chemical Sciences not elsewhere classified intraperitoneal injection ), apoptotic protein chop molecular chaperone properties renal injury caused renal function caused protein aggregation induced protective mechanisms found div >< p apoptotic cell death acute kidney injury inhibit er stress induces er stress renal protection provided histone hyperacetylation provides hdac inhibitors used commonly used model hdac inhibitor effects prevent er stress protective effects cell death er stress renal damage histone hyperacetylation various mechanisms chemical chaperone induced model histone deacetylation histone deacetylase work demonstrated vitro </ tunicamycin model structural damage steroidal anti significant increase primarily due nucleoside antibiotic main objective inflammatory drugs including antibiotics endoplasmic reticulum data suggest 50 mg 5 mg 1 g
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Wild type mice were given tunicamycin (TM; 0.5 mg/kg I.P) for three days with or without vorinostat (vor; 50 mg/kg/day) or 4-phenylbutyrate (PBA; 1 g/kg/day).

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