title: The protective effect of baicalin against renal ischemia-reperfusion injury through inhibition of inflammation and apoptosis.
abstract: BACKGROUND
  Renal ischemia-reperfusion injury (IRI) increases the rates of acute kidney failure, delayed graft function, and early mortality after kidney transplantation. The pathophysiology involved includes oxidative stress, mitochondrial dysfunction, and immune-mediated injury. The anti-oxidation, anti-apoptosis, and anti-inflammation properties of baicalin, a flavonoid glycoside isolated from Scutellaria baicalensis, have been verified. This study therefore assessed the effects of baicalin against renal IRI in rats.
  
  
  METHODS
  Baicalin was intraperitoneally injected 30 min before renal ischemia. Serum and kidneys were harvested 24 h after reperfusion. Renal function and histological changes were assessed. Markers of oxidative stress, the Toll-like receptor (TLR)2 and TLR4 signaling pathway, mitochondrial stress, and cell apoptosis were also evaluated.
  
  
  RESULTS
  Baicalin treatment decreased oxidative stress and histological injury, and improved kidney function, as well as inhibiting proinflammatory responses and tubular apoptosis. Baicalin pretreatment also reduced the expression of TLR2, TLR4, MyD88, p-NF-κB, and p-IκB proteins, as well as decreasing caspase-3 activity and increasing the Bcl-2/Bax ratio.
  
  
  CONCLUSIONS
  Baicalin may attenuate renal ischemia-reperfusion injury by inhibiting proinflammatory responses and mitochondria-mediated apoptosis. These effects are associated with the TLR2/4 signaling pathway and mitochondrial stress.
authors.forename: Miao
authors.initials: M
authors.lastname: Lin
authors.forename: Long
authors.initials: L
authors.lastname: Li
authors.forename: Liping
authors.initials: L
authors.lastname: Li
authors.forename: Gaurab
authors.initials: G
authors.lastname: Pokhrel
authors.forename: Guisheng
authors.initials: G
authors.lastname: Qi
authors.affiliation: Department of Urology, Fudan University Zhongshan Hospital, Shanghai, China. rong.ruiming@zs-hospital.sh.cn.
authors.forename: Ruiming
authors.initials: R
authors.lastname: Rong
authors.forename: Tongyu
authors.initials: T
authors.lastname: Zhu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000378:metabolism; D005419:Flavonoids / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use*; D007249:Inflammation / Q000097:blood / Q000201:enzymology / Q000378:metabolism / Q000517:prevention & control; D007511:Ischemia / Q000097:blood / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D007668:Kidney / Q000187:drug effects / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D007674:Kidney Diseases / Q000097:blood / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D008297:Male; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D053594:Myeloid Differentiation Factor 88 / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000097:blood / Q000378:metabolism / Q000473:pathology* / Q000517:prevention & control*; D015398:Signal Transduction / Q000187:drug effects; D051193:Toll-Like Receptors / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D005419:Flavonoids; C507781:Myd88 protein, rat; D053594:Myeloid Differentiation Factor 88; D016328:NF-kappa B; D051193:Toll-Like Receptors; D051028:bcl-2-Associated X Protein; C038044:baicalin; D053148:Caspase 3