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1                            Pretreatment with cobalt protoporphyrin 24 h before LPS challenge normaliz
2 raperitoneally administered the HO-1 inducer cobalt protoporphyrin (3 mg/kg CoPP) with and without th
3 omodulatory peptides are similar to those of cobalt-protoporphyrin, a known up-regulator of HO-1.
4                                          The cobalt protoporphyrin-activated hBVR phosphorylated a th
5 ic administration of the HO inducers heme or cobalt protoporphyrin and the effect of HO inhibition us
6 O-1 in a rat cardiac I/R injury model, using cobalt protoporphyrin (CoPP) as HO-1 inducer and zinc pr
7 er induction of HO-1 after administration of cobalt protoporphyrin (CoPP) can prevent the development
8 nd induction of heme oxygenase-1 (HO-1) with cobalt protoporphyrin (CoPP) markedly attenuated the dev
9 ally obese Zucker rats with the HO-1 inducer cobalt protoporphyrin (CoPP) or with adenoviral HO-1 (Ad
10                                              Cobalt protoporphyrin (CoPP) reduces food intake and bod
11                                      We used cobalt protoporphyrin (CoPP) treatment to evaluate the e
12 ates EBOV replication, we treated cells with cobalt protoporphyrin (CoPP), a selective HO-1 inducer,
13                                              Cobalt protoporphyrin (CoPP), a well known heme oxygenas
14                                              Cobalt protoporphyrin (CoPP)-induced HO-1 overexpression
15  in mice in which NRF2/HO-1 was induced with cobalt protoporphyrin (CoPP).
16 al-mediated overexpression or induction with cobalt protoporphyrin (CoPP, a potent HO-1 inducer), pre
17  treated with the pharmacologic HO-1 inducer cobalt protoporphyrin demonstrated amelioration of activ
18 and Hb(+)CN), ferrous (HbCO and HbO(2)), and cobalt-protoporphyrin derivatives of Hb, whereas globin
19                    Here, we demonstrate that cobalt protoporphyrin IX (CoPP) and zinc protoporphyrin
20 tion of HO-1 expression by administration of cobalt protoporphyrin IX (CoPPIX) to the graft donor res
21 , Escherichia coli BL21(DE3), biosynthesizes cobalt protoporphyrin IX (CoPPIX) under iron-limited, co
22 ombined with induction of HO-1 expression by cobalt protoporphyrin IX (CoPPIX).
23   Some rats were treated with HO-1 activator cobalt protoporphyrin IX chloride (Copp; 25 mg/kg body w
24                             The HO-1 inducer cobalt protoporphyrin IX diminished proinflammatory cyto
25         Furthermore, upregulation of HO-1 by cobalt protoporphyrin IX diminished the production of TN
26 ive sperm whale myoglobin reconstituted with cobalt protoporphyrin IX have been determined by x-ray c
27                             The HO-1 inducer cobalt protoporphyrin IX more efficiently attenuated PGE
28         In contrast, HO-1 agonists hemin and cobalt protoporphyrin IX significantly increased DAF pro
29 ection, HO-1 induction with metalloporphyrin cobalt protoporphyrin IX significantly reduces the loss
30 eudomallei Pharmacological administration of cobalt protoporphyrin IX to mice resulted in an enhanced
31                          Concomitantly, upon cobalt protoporphyrin IX treatment, there is a significa
32 tivation of transcription by hemoglobin and (cobalt protoporphyrin IX) globin but not by apoglobin or
33                               Interestingly, cobalt protoporphyrin IX, an HO-1 inductor, increased th
34   HO-1 was induced in vivo by treatment with cobalt protoporphyrin IX, starting at week 5 or 12 of mi
35 a heme binding protein, heme oxygenase, with cobalt-protoporphyrin IX, with good activity for the pho
36  events associated with heme transport since cobalt-protoporphyrin IX-hemopexin, which binds to the r
37 pharmacologic induction of HMOX-1 in vivo by cobalt protoporphyrin-IX treatment eradicated intestinal
38 terfering RNA or by treatment with 5 mumol/L cobalt protoporphyrin or heme (known inducers of HO-1) d
39 ilencing the Bach1 gene or by treatment with cobalt protoporphyrin or heme, decreases HCV replication
40  HO-2 (-/-) mice by weekly administration of cobalt protoporphyrin prevented the increase in plasma c
41    Prior induction of HO-1 expression, using cobalt-protoporphyrin, protected RAW264.7 cells against
42                                       CO and cobalt protoporphyrin suppressed colonic IL-1beta, TNF,
43 anol feeding, with or without treatment with cobalt protoporphyrin, to induce HO-1.