Hypoxia-Induced Kidney Injury in Newborn Rats

Abstract

Exposure to hypoxia during the early postnatal period can have adverse effects on vital organs. Neonatal Sprague–Dawley rats housed in a hypoxic chamber were compared to those in a normoxic chamber from postnatal days 0 to 7. Arterial blood was collected to evaluate renal function and hypoxia. Kidney morphology and fibrosis were evaluated using staining methods and immunoblotting. In the kidneys of the hypoxic group, protein expressions of hypoxia-inducible factor-1 were higher than those in the normoxic group. Hypoxic rats had higher levels of hematocrit, serum creatinine, and lactate than normoxic rats. Body weight was reduced, and protein loss of kidney tissue was observed in hypoxic rats compared to normoxic rats. Histologically, hypoxic rats showed glomerular atrophy and tubular injury. Renal fibrosis with collagen fiber deposition was observed in the hypoxic group. The expression of nicotinamide adenine dinucleotide phosphate oxidases was enhanced in the kidneys of hypoxic rats. Proteins involved in apoptosis were upregulated in the kidneys of hypoxic rats. An increase in the expression of pro-inflammatory cytokines was also observed in the kidneys of hypoxic rats. Hypoxic kidney injury in neonatal rats was associated with oxidative stress, inflammation, apoptosis, and fibrosis.

Propranolol Alleviates Cardiac Injury After Acute Catecholamine Infusion Through p38-MAPK Pathways

“…Protein extraction and Western blot analysis were performed as previously described. 7 The primary antibodies used included anti-GAB1 (1:500, #M01989; Boster Biological Technology), anti-cardiac troponin T (TnT) (1:500, ARG10451; Arigo Biolaboratories Corp, Hsinchu, Taiwan), antisoluble interleukin 1 receptor-like 1 (ST2) (1:1000, 11920-1-AP; Proteintech Group, Inc, Rosemont, IL), phospho-p38 MAPK (Thr180/Tyr182) (1:1000, 9211; Cell Signaling Technology), p38 MAPK (1:1000, 9212; Cell Signaling Technology), phospho-p38 MAPK (D-8) (1:100, sc-7973; Santa Cruz Biotechnology, Dallas, TX), phospho-p38 alpha MAPK (1:1000, 9218; Cell Signaling Technology), phospho-MAPK11 (Thr180, Tyr182) (1:1000, BS-5506R; Bioss Antibodies, Boston, MA), phospho-p38 beta MAPK (1:1000, sc-390984; Santa Cruz Biotechnology), phospho-SAPK/JNK (Thr183/Tyr185) (1:1000, 4668S; Cell Signaling Technology), SAPK/JNK (1:1000, 9252S; Cell Signaling Technology), antinuclear factor-κB (1:1000, 10745-1-AP; Proteintech Group, Inc), anti-inducible nitric oxide synthase (iNOS) (1:8000, 610432; BD Biosciences, East Rutherford, NJ), anti-p22phox (1:1000, sc271968; Santa Cruz Biotechnology), anti-p47phox (1:500, sc17845; Santa Cruz Biotechnology), anti-NOX2 (ab129068; Abcam, Cambridge, United Kingdom), anti-NOX4 (1:1000, 14347-1-AP; Proteintech Group, Inc), anti-caspase 8 (1:1000, ARG57632; Arigo Biolaboratories Corp), anti-caspase 9 (1:1000, GTX112888; GeneTex, Irvine, CA), anti-cleaved caspase 3 (1:1000, 9664; Cell Signaling Technology), anti-FGF-23 (FGF-23) (1:1000, LS-C411984; Lifespan Biosciences, Seattle, WA), anti-alpha smooth muscle actin (alpha-SMA) (1:1000, ab5694; Abcam), antimatrix metalloproteinase 9 (MMP9) (1:1000, ab38898; Abcam), antitumor necrosis factor-alpha (TNF-alpha) (1:1000, PA1079; Boster Biological Technology), antihigh mobility group box 1 (high mobility group box 1) (1:1000, ab79823; Abcam), phospho-protein kinase B (Akt) (Ser473) (1:1000, 4060; Cell Signaling Technology), phospho-Akt (Thr308) (1:1000, 9275; Cell Signaling Technology), Akt (1:1000, 9272, Cell Signaling Technology), phospho-p44/42 MAPK (Erk1/2) (Thr202/Tyr204) (1:1000, 4370; Cell Signaling Technology), p44/42 MAPK (Erk1/2) (1:1000, 9102; Cell Signaling Technology), and anti-GAPDH (1:2000, 60004-1-Ig; Proteintech Group, Inc). The secondary antibodies used were anti-mouse (C04001; Croyez Bioscience, Taipei, Taiwan) and anti-rabbit (C04003; Croyez Bioscience).…”

“…Protein extraction and Western blot analysis were performed as previously described. 7 The primary antibodies used included anti-GAB1 (1:500, #M01989; Boster Biological Technology), anti-cardiac troponin T (TnT) (1:500, ARG10451; Arigo Biolaboratories Corp, Hsinchu, Taiwan), antisoluble interleukin 1 receptor-like 1 (ST2) (1:1000, 11920-1-AP; Proteintech Group, Inc, Rosemont, IL), phospho-p38 MAPK (Thr180/Tyr182) (1:1000, 9211; Cell Signaling Technology), p38 MAPK (1:1000, 9212; Cell Signaling Technology), phospho-p38 MAPK (D-8) (1:100, sc-7973; Santa Cruz Biotechnology, Dallas, TX), phospho-p38 alpha MAPK (1:1000, 9218; Cell Signaling Technology), phospho-MAPK11 (Thr180, Tyr182) (1:1000, BS-5506R; Bioss Antibodies, Boston, MA), phospho-p38 beta MAPK (1:1000, sc-390984; Santa Cruz Biotechnology), phospho-SAPK/JNK (Thr183/Tyr185) (1:1000, 4668S; Cell Signaling Technology), SAPK/JNK (1:1000, 9252S; Cell Signaling Technology), antinuclear factor-kB (1:1000, 10745-1-AP; Proteintech Group, Inc), anti-inducible nitric oxide synthase (iNOS) (1:8000, 610432; BD Biosciences, East Rutherford, NJ), anti-p22phox (1:1000, sc271968; Santa Cruz Biotechnology), anti-p47phox…”

Oxygen Variations—Insights into Hypoxia, Hyperoxia and Hyperbaric Hyperoxia—Is the Dose the Clue?

“…Hyperoxia during the neonatal period impairs renal tubular development. Human and animal studies have demonstrated that neonatal hyperoxia increases oxidative stress and induces glomerular and tubular injuries, which are manifested as renal corpuscle enlargement, renal tubular necrosis, interstitial inflammation, and kidney fibrosis during the perinatal period [34][35][36].…”