superoxide

dismutase
(SOD)

Made by: Juan Felipe Duarte Zambrano athione glutamyltransferase

(GSH) (GGT)
jduartez@unal.edu.co

C.C. 1010077553 Amplify grain DAMPs as acute phase

inflammation by protein serum amyloid
Antioxidant
glia A BY PAMPs
enzymes
glutathione glutathione glutathione or DAMPs
catalase
reductase peroxidase S-transferase (such as
(CAT)
(GSSG-Rd) (GSH-Px) (GST) ROS)

Neuroprotective
References effects of IL-1B
Brain NLRP3 binds with Activation Production
suprresion in when Formation of the
ASC and of of IL-1B
1.Minutoli L, Puzzolo D, Rinaldi M, Irrera N, Marini H, Arcoraci V, et al. ROS-Mediated NLRP3 Inflammasome Activation in Brain, infarction activated inflamasome
procaspase 1 caspase 1 and IL-18
Heart, Kidney, and Testis Ischemia/Reperfusion Injury. Oxid Med Cell Longev. 2016;2016.
NLP3 is a The most
potential sensitive ROS-Mediated NLRP3 TNF alfa
therapeutic targed organ to I/R Imbalance between Inflammasome Activation in Gene
Oxidative NOD like signaling
in Stroke injury free radical production NLRP3 induced
stress Brain,Heart, Kidney, and Testis receptors induces
and neutralization Ischemia/Reperfusion Injury (1) by NFkB Proinflammatory
NFkB Pyroptosis Apoptosis Autophagy
ROS induce
lipid
peroxidation
Induces pro
Heart IL-1B and pro activated
IL-18 genes Non by cell
Apoptosis with caspase From bacterial
Reduction in arterial blood canonical wall
Ischemia 4 and 5 phagocytosis
suplly pathway ligands
like LPS

Necrosis

Changes Restoration of perfusion and re Neutrophil

Reperfusion
in calcium oxygenation infiltration recognition of
Canonical
caspase 1 general cellular like ROS production
pathway
stress
Kidney
Damage
Early and late
Ischemic reperfusion to
phase
is a common cause of ischemic
acutre renal failure tissue
Restoration of blood flow as soon as possible is still the best
approach to reduce the ischemia / reperfusion injury
Free
Hystological Interference Inflammatory Adenyl cyclase radicals
changes up to 24 - ROS and AMPc are
in cellular ion response to cell are
75 hours accumulation reduced
Protection homeostasis death produced
against IL-18 KO mice
ischemic reduce tubular
reperfusion damage
injury

Hydrogen
Hydroxyl peroxide Superoxide TRX and
radical anion TRXIP
Susceptible to complex
Epithelial cells of NLRP3
ischemic Outer renal
the S3 segment of inflammasome
reperfusion medulla
the proximal tubule activation
injury
produced
by Pathologyc
Normal
status with high
status
concentrations
of ROS
May sense Other
presence of indirect generated by
ROS activators mitochondria as Generated by
result of O2 lipoxygenase and TXNIP is
metabolism cclooxygenase reduced
Testis and the complex
Pediatric dissociate and
I/R injury torsion Testis binded
population Produced by TXNIP activates
and lesion with TRX
mitochondria NLRP3

Enzymatic By normal By abnormal

antioxidants, ptotect mitochondria mitochondria
germinal cells from
ROS damage