Dimethylsulfoxide (DMSO) treatment reduces infarction volume after permanent focal cerebral ischemia in rats

Shimizu, Shigetoshi; Simon, Roger P.; Graham, Steven H.

doi:10.1016/s0304-3940(97)00915-4

Cited by 69 publications

(47 citation statements)

References 21 publications

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“…It causes histamine release by mast cells and this effect is probably responsible for the vasodilation (14)(15)(16). It is a free radical scavenger and thus may reduce oxidative stress after ischaemia (15)(16)(17). DMSO has local anesthetic effects and thus would improve ischaemic injury by effects on cell excitation (17).…”

Section: Discussionmentioning

confidence: 99%

Prevention of Wound Edge Necrosis by Local Application of Dimethylsulfoxide

Çelen¹,

Yıldırım²,

Berberoğlu³

2005

Acta Chirurgica Belgica

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Section: Discussionmentioning

confidence: 99%

Prevention of Wound Edge Necrosis by Local Application of Dimethylsulfoxide

Çelen¹,

Yıldırım²,

Berberoğlu³

2005

Acta Chirurgica Belgica

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“…Atypical antipsychotics, Src and cortical injury J Dickerson and FR Sharp modest antioxidant that can protect against stroke and other types of brain injury (Shimizu et al, 1997). In addition, we have previously shown that another antioxidant 1,3-dimethylthiourea markedly protects against the neuronal injury produced by systemic MK-801 (Rajdev et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Atypical Antipsychotics and a Src Kinase Inhibitor (PP1) Prevent Cortical Injury Produced by the Psychomimetic, Noncompetitive NMDA Receptor Antagonist MK-801

Dickerson

Sharp

2005

Neuropsychopharmacol

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Noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonists such as phencyclidine, ketamine, and MK-801 produce schizophrenia-like psychosis in humans. The same NMDA antagonists injure retrosplenial cortical neurons in adult rats. We examined the effects of atypical antipsychotics and an inhibitor of nonreceptor tyrosine kinase pp60 (Src) on the cortical injury produced by MK-801. An atypical antipsychotic (either clozapine, ziprasidone, olanzapine, quetiapine, or risperidone) or vehicle was administered to adult female Sprague-Dawley rats. PP1 (Src inhibitor), PP3 (nonfunctional analog of PP1) or vehicle (DMSO) was administered to another group of animals. After pretreatment, animals were injected with MK-801, killed 24 h after the MK-801, and injury to retrosplenial cortex assessed by neuronal Hsp70 protein expression. All atypical antipsychotics examined significantly attenuated MK-801-induced cortical damage. PP1 protected compared to vehicle, whereas PP3 did not protect. The ED50s (decrease injury by 50%) were as follows: PP1 o0.1 mg/kg; olanzapine 0.8 mg/kg; risperdal 1 mg/kg; clozapine 3 mg/kg; ziprasidone 32 mg/kg; and quetiapine 45 mg/kg. The data show that the atypical antipsychotics tested as well as a Src kinase inhibitor prevent the injury produced by the psychomimetic MK-801, and the potency of the atypical antipsychotics for preventing cortical injury was roughly similar to the potency of these drugs for treating psychosis in patients.

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“…Our findings suggest that unexpected biological activities of DMSO can cause critical interference in the evaluation of anti-allergic activities of chemicals dissolved in it, unless the final concentration of DMSO is carefully adjusted. In addition, these results might explain the anti-inflammatory properties of DMSO which could not be explained before (Brayton, 1986;Jacob and Wood, 1967;RandLuby et al, 1996;Shimizu et al, 1997).…”

Section: Discussionmentioning

confidence: 83%

Distinct effects on M2-type pyruvate kinase are involved in the dimethylsulfoxide-induced modulation of cellular proliferation and degranulation of mast cells

Koo

Kim

2009

Arch. Pharm. Res.

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Dimethylsulfoxide (DMSO), a universal solvent, is frequently used to dissolve various classes of chemicals for the evaluation of their biological activities. In one such evaluation, we noticed that DMSO itself caused cellular proliferation and interfered with high affinity IgE receptor (FcepsilonRI)-mediated degranulation of mast cells. DMSO caused cellular proliferation of RBL-2H3 cells by phosphorylating both extracellular-signal regulated kinase (ERK) and M2-type pyruvate kinase (M2PK) through which the enzymatic activity of M2PK was reduced. Allergenic activation of FcepsilonRI caused the tyrosine phosphorylations of signaling components of FcepsilonRI, such as Syk, PLCgamma1, PLCgamma2, ERK, and M2PK. In these allergenic activated RBL-2H3 cells, DMSO specifically inhibited FcepsilonRI-mediated tyrosine phosphorylation of M2PK, blocked FcepsilonRI-mediated inhibition of the enzymatic activity of M2PK, and then inhibited FcepsilonRI-mediated degranulation. These results suggest that DMSO causes cellular proliferation and mast cell degranulation through differential modulation of M2PK in resting and allergenic activated cells.

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Dimethylsulfoxide (DMSO) treatment reduces infarction volume after permanent focal cerebral ischemia in rats

Cited by 69 publications

References 21 publications

Prevention of Wound Edge Necrosis by Local Application of Dimethylsulfoxide

Prevention of Wound Edge Necrosis by Local Application of Dimethylsulfoxide

Atypical Antipsychotics and a Src Kinase Inhibitor (PP1) Prevent Cortical Injury Produced by the Psychomimetic, Noncompetitive NMDA Receptor Antagonist MK-801

Distinct effects on M2-type pyruvate kinase are involved in the dimethylsulfoxide-induced modulation of cellular proliferation and degranulation of mast cells

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