Protective effect of vitamin D3 analogues on endotoxin shock in mice

Horiuchi, Hideki; Nagata, Ikuo; Komoriya, Keiji

doi:10.1007/bf01986584

Cited by 48 publications

(29 citation statements)

References 24 publications

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“…In contrast to the studies by Horiuchi 6 and Asakura 7 we were unable to demonstrate a protective effect of 1,25-vit D treatment in the LPS induced sepsis.…”

Section: Discussioncontrasting

confidence: 99%

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Effect of 1,25-dihydroxy-vitamin D₃ in experimental sepsis

Möller¹,

Laigaard²,

Ølgaard³

et al. 2007

Int. J. Med. Sci.

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Background: In addition to the regulation of calcium homeostasis, vitamin D affects the cellular immune system, targets the TNF-α pathway and increases vasoconstrictor response to angiotensin II. We therefore examined the effect of 1,25-dihydroxy-vitamin D 3 on coagulation and organ failure in experimental sepsis in the rat. Methods: Three series of placebo-controlled studies were conducted. All rats were pre-treated with daily SC injections of 1,25-dihydroxy-vitamin D 3 100 ng/kg or placebo vehicle for 3 days. In study 1, sepsis was accomplished by abdominal surgery comprising a coecal ligation and puncture with a 1,2 mm needle, or sham surgery. In study 2, the rats had a single IP injection of lipopolysaccharide from E. Coli 0111:B4 (LPS) 8 mg/kg, or placebo. In study 3, an hour-long IV infusion of LPS 7 mg/kg, or placebo was given. Results: All three models of sepsis showed significant effects on coagulation and liver function with reduced thrombocyte count and prothrombin time together with elevated ALT and bilirubin (p<0.05) as compared to controls. In study 1, the vitamin D treated rats maintained normal platelet count, whereas the vehicle treated rats showed a significant reduction (p<0.05). This effect of vitamin D on platelets was not found in the LPS-treated groups. We found no significant differences between vitamin D and placebo-treated rats with regards to liver function. Conclusion:The present data suggest a positive modulating effect of 1,25-dihydroxy-vitamin D 3 supplementation on sepsis-induced coagulation disturbances in the coecal ligation and puncture model. No such effect was found in LPS-induced sepsis.

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“…In contrast to the studies by Horiuchi 6 and Asakura 7 we were unable to demonstrate a protective effect of 1,25-vit D treatment in the LPS induced sepsis.…”

Section: Discussioncontrasting

confidence: 99%

“…We, therefore, decided to duplicate the experimental protocols used by Horiuchi 6 and Asakura 7 but also to add an examination of a model of abdominal sepsis. To probe the possibility that 1,25-vit D could have therapeutic potential within pharmacologically safe doses, a previously validated dose of 1,25-vit D was chosen 8 .…”

Section: Discussionmentioning

confidence: 99%

Effect of 1,25-dihydroxy-vitamin D₃ in experimental sepsis

Möller¹,

Laigaard²,

Ølgaard³

et al. 2007

Int. J. Med. Sci.

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“…40 1,25-VD has been found to inhibit endotoxin shock through regulation of free radical formation in mice. 41 1,25-VD enhanced intracellular GSH pools, and thus decreased free radical formation in rat primary astrocytes. 42 Furthermore, vitamin D has also been reported to reduce oxidative stress by upregulating antioxidant systems, including GSH, GPx and superoxide dismutase in rats.…”

Section: Discussionmentioning

confidence: 87%

Protective role of 1α, 25‐dihydroxyvitamin D₃ against oxidative stress in nonmalignant human prostate epithelial cells

Bao

Ting

Hsu

et al. 2008

Intl Journal of Cancer

146

108

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Overproduction of reactive oxygen species (ROS), through either endogenous or exogenous sources, could induce DNA damage, and accumulation of DNA damage might lead to multistep carcinogenesis. The antioxidative effects of vitamin D have been suggested by epidemiological and many in vitro and in vivo laboratory studies. While exploring the antioxidative effects of vitamin D in prostate cells, we found that the active form of vitamin D, 1a, 25-dihydroxyvitamin D 3 (1,25-VD), can protect nonmalignant human prostate epithelial cell lines, BPH-1 and RWPE-1, but not malignant human prostate epithelial cells, CWR22R and DU 145, from oxidative stress-induced cell death. Glucose-6-phosphate dehydrogenase (G6PD), a key antioxidant enzyme, was dose-and time-dependently induced by 1,25-VD. Mechanistic studies using chromatin immunoprecipitation (ChIP) assay revealed that a direct repeat-3 (DR3) vitamin D response element located in the first intron of the G6PD genome can be bound by liganded vitamin D receptor, thereby regulating G6PD gene expression. Increasing G6PD activity and glutathione level by 1,25-VD can scavenge cellular ROS. Moreover, the protective effects of 1,25-VD were abolished by dehydroepiandrosterone, a noncompetitive inhibitor of G6PD activity. Together, our results showed that 1,25-VD can protect nonmalignant prostate cells from oxidative stress-induced cell death by elimination of ROS-induced cellular injuries through transcriptional activation of G6PD activity. The antioxidative effect of vitamin D strengthens its roles in cancer chemoprevention and adds to a growing list of beneficial effects of vitamin D against cancer.

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“…Therefore, it is possible to speculate that calcitriol and other vitamin D derivatives might have some beneficial effect in certain situations of abnormal cytokine release. For instance, given its capability to de crease TNF secretion both in vitro and ex vivo, it would be interesting to explore its usefulness to ameliorate the symp toms of the 'cytokine release syndrome' associated with the use of OKT3 antibodies [29], A beneficial effect of calcitriol in vivo has also been recently reported in some animal models of autoimmune disease [30] and endotoxic shock [31].…”

Section: Discussionmentioning

confidence: 99%

Vitamin D Therapy Modulates Cytokine Secretion in Patients with Renal Failure

Riancho

Zarrabeitia

Francisco

et al. 1993

Nephron

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In studies in vitro calcitriol (1,25-dihydroxyvitamin D₃) inhibits lymphocyte proliferation and modulates several monocyte functions, including the secretion of prostaglandins and monokines. However its effects on monokine production in vivo are not known. Therefore we studied the secretion of interleukin (IL)-1, IL-6 and tumor necrosis factor (TNF) by peripheral blood mononuclear cells (PBMC) from 7 patients on periodic hemodialysis, before and after oral treatment with calcitriol (0.5 μg daily) for 1 month. Calcitriol therapy resulted in significant increases in the phorbol myristate acetate (PMA)-induced secretion of IL-1 and IL-6 (p = 0.04 and 0.03, respectively). This was a transient effect, observable by day 7 of therapy, but no longer evident by day 30. However, calcitriol induced a progressive reduction of TNF secretion (down to 53% of control values by day 30, p = 0.02). There were no correlations between the individual changes in calcium/PTH and cytokine release. These results show that doses of calcitriol within the therapeutic range induce marked changes in cytokine secretion by PBMC from uremic patients.

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Protective effect of vitamin D3 analogues on endotoxin shock in mice

Cited by 48 publications

References 24 publications

Effect of 1,25-dihydroxy-vitamin D₃ in experimental sepsis

Effect of 1,25-dihydroxy-vitamin D₃ in experimental sepsis

Protective role of 1α, 25‐dihydroxyvitamin D₃ against oxidative stress in nonmalignant human prostate epithelial cells

Vitamin D Therapy Modulates Cytokine Secretion in Patients with Renal Failure

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Protective effect of vitamin D3 analogues on endotoxin shock in mice

Cited by 48 publications

References 24 publications

Effect of 1,25-dihydroxy-vitamin D3 in experimental sepsis

Effect of 1,25-dihydroxy-vitamin D3 in experimental sepsis

Protective role of 1α, 25‐dihydroxyvitamin D3 against oxidative stress in nonmalignant human prostate epithelial cells

Vitamin D Therapy Modulates Cytokine Secretion in Patients with Renal Failure

Contact Info

Product

Resources

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Effect of 1,25-dihydroxy-vitamin D₃ in experimental sepsis

Effect of 1,25-dihydroxy-vitamin D₃ in experimental sepsis

Protective role of 1α, 25‐dihydroxyvitamin D₃ against oxidative stress in nonmalignant human prostate epithelial cells