Biomedical subjects

Hisae Nishii

Publications and source records attributed to Hisae Nishii.

4 recordsLinked to original sources

PubMed2006

The hypothalamo-pituitary axis responses to lipopolysaccharide-induced endotoxemia in mice lacking inducible nitric oxide synthase.

Nitric oxide (NO) generated by inducible NO synthase (iNOS) may be implicated in the biological responses of the central nervous system to immune stimuli. To elucidate the role of iNOS in the hypothalamo-pituitary axis in responses to endotoxemia, using iNOS knockout (KO) mice, we examined the levels of c-fos, a neural activational marker, and corticotropin-releasing hormone (CRH) gene transcription in the paraventricular nucleus (PVN) and central amygdala (CeAMY) during lipopolysaccharide (LPS)-induced endotoxemia. In addition, the serum adrenocorticotropic hormone (ACTH) levels were also examined during endotoxemia. Following the intraperitoneal administration of LPS (1 mg/kg), the levels of the c-fos gene expression significantly increased in the PVN and the CeAMY regardless of the genotype. However, the disruption of the iNOS gene resulted in a significant decrease in the c-fos gene induction in the PVN in comparison to that observed in control mice. LPS administration caused a significant increase in CRH mRNA levels in the PVN and CeAMY regardless of genotype. However, the LPS-induced upregulation of CRH mRNA was significantly attenuated in the PVN of iNOS KO mice in comparison to that in the control mice. In contrast, no such genotype differences in the neural activity or CRH gene transcription were observed in the CeAMY. The serum ACTH responses to LPS were also significantly blunted in the iNOS KO mice in comparison to the control mice. These results suggest that iNOS-derived NO may therefore play a stimulatory role in the activity of the hypothalamo-pituitary axis during endotoxemia.

Adrenocorticotropic Hormone↗

PubMed2006

Up-regulation of interleukin-6 gene expression in cyclophosphamide-induced cystitis in mice: An in situ hybridization histochemical study.

AIM: To determine the time course and the cellular sources of interleukin (IL)-6 in the bladder during experimental cystitis, the expression of the IL-6 gene and IL-6 protein was examined in the bladder during cyclophosphamide (CP)-induced cystitis. METHODS: Mice were killed at 0, 1, 2, 6, 12 and 48 h after the intraperitoneal administration of 0.9% saline containing either CP (200 mg/kg) or saline. The expression of IL-6 gene and IL-6 protein were detected using in situ hybridization histochemistry and immunocytochemistry, respectively. RESULTS: In situ hybridization histochemistry showed that IL-6 gene expression was significantly up-regulated in the bladder at 1 h in comparison to that at 0 h after CP administration. The levels of IL-6 gene expression peaked at 6 h after CP administration and then declined thereafter. In contrast, only a few IL-6 transcripts were expressed in the bladder but they remained unchanged following the administration of saline at all time points examined. The IL-6 transcripts were predominantly distributed in the perivascular area of the submucosal layers during CP-induced cystitis. Immunocytochemistry demonstrated IL-6 immunoreactivity in the spindle-shaped cells located in the vicinity of the dilated vessels of the submucosal layers during CP-induced cystitis. CONCLUSION: IL-6 gene expression was up-regulated in the submucosal layer of the bladder and peaked at 6 h after CP administration, suggesting that the primary source of IL-6 may be fibroblasts in the bladder during CP-induced cystitis.

Animals↗

PubMed2005

Involvement of estrogen in the pathogenesis of cyclophosphamide-induced cystitis in rats.

We examined the effects of ovariectomy and castration on the histology of cyclophosphamide (CP)-induced cystitis in rats. The animals were injected with CP (100 mg/kg) or saline intraperitoneally twice with an intervening 4 d and were euthanized at 1 or 2 wk after the initial CP administration. Saline treatment did not cause an apparent histological change in the bladder regardless of surgery, i.e., ovariectomy, castration, and sham-operation. CP treatment resulted in submucosal edema, urothelial damage, hemorrhage, and leukocyte infiltration in the bladder at 1 wk after the initial CP administration regardless of surgery. However, these histological changes were more severe in ovariectomized rats than in the sham-operated rats. In contrast, there were no significant differences in CP-induced histological changes in the bladder between castrated and sham-operated groups. We further examined the role of estrogen and progesterone on the CP-induced histology in the bladder by the replacement with estrogen only or estrogen plus progesterone for 2 wk in overiectomized rats. Estrogen treatment ameliorated CP-induced histological changes compared to oil treatment, whereas estrogen plus progesterone treatment did not produce any differences in the histology of the bladder compared to estrogen treatment. These results suggest that estrogen may play a role in the pathogenesis of bladder inflammation.

Animals↗

PubMed2005

[Tests for syphilis].

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