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Titolo:
Differential effects of dexamethasone treatment on lipopolysaccharide-induced testicular inflammation and reproductive hormone inhibition in adult rats
Autore:
Gow, RM; OBryan, MK; Canny, BJ; Ooi, GT; Hedger, MP;
Indirizzi:
Monash Univ, Monash Inst Reprod & Dev, Clayton, Vic 3168, Australia MonashUniv Clayton Vic Australia 3168 Dev, Clayton, Vic 3168, Australia Prince Henrys Inst Med Res, Clayton, Vic 3168, Australia Prince Henrys Inst Med Res Clayton Vic Australia 3168 Vic 3168, Australia
Titolo Testata:
JOURNAL OF ENDOCRINOLOGY
fascicolo: 1, volume: 168, anno: 2001,
pagine: 193 - 201
SICI:
0022-0795(200101)168:1<193:DEODTO>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
PITUITARY-ADRENAL AXIS; TUMOR-NECROSIS-FACTOR; HUMAN CHORIONIC-GONADOTROPIN; LEYDIG-CELL STEROIDOGENESIS; ACUTE REGULATORY PROTEIN; MESSENGER-RIBONUCLEIC-ACID; LEVELS IN-VIVO; TESTOSTERONE SECRETION; RHEUMATOID-ARTHRITIS; GENE-EXPRESSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Hedger, MP Monash Med Ctr, Monash Inst Reprod & Dev, Clayton, Vic 3168, Australia Monash Med Ctr Clayton Vic Australia 3168 Vic 3168, Australia
Citazione:
R.M. Gow et al., "Differential effects of dexamethasone treatment on lipopolysaccharide-induced testicular inflammation and reproductive hormone inhibition in adult rats", J ENDOCR, 168(1), 2001, pp. 193-201

Abstract

A single intraperitoneal injection of Lipopolysaccharide (LPS) causes a biphasic suppression of testicular steroidogenesis in adult rats, with inhibition at 6 h and 18-24 h after injection. The inhibition of steroidogenesis is independent of the reduction in circulating LH that also occurs after LPS treatment, indicating a direct effect of inflammation at the Leydig cell level. The relative contributions to this inhibition by intratesticular versus systemic responses to inflammation, including the adrenal glucocorticoids, was investigated in this study. Adult male Wistar rats (eight/group) received injections of LPS (0.1 mg/kgi.p.), dexamethasone (DEX; 50 mug/kg i.p.), LPS and DEX, or saline only (controls), and were killed 6 h, 18 h and 72 h later. Treatment with LPS stimulated body temperature and serum corticosterone levels measured 6 h later. Administration of DEX had no effect on body temperature, but suppressed serum corticosterone levels. At the dose used in this study, DEX alone had noeffect on serum LH or testosterone at any time-point. Expression of mRNA for interleukin-1 beta (IL-1 beta), the principal inflammatory cytokine, wasincreased in both testis and liver of LPS-treated rats. Serum LH and testosterone levels were considerably reduced at 6 h and 18 h after LPS treatment, and had not completely recovered by 72 h. At 6 h after injection, DEX inhibited basal IL-1 beta expression and the LPS-induced increase of IL-1 beta mRNA levels in the liver, but had no effect on IL-1 beta in the testis. The effects of DEX on IL-1 beta levels in the liver were no longer evident by 18 h. In LPS-treated rats, DEX caused a significant reversal of the inhibition of serum LH and testosterone at 18 h, although not at 6 h or 72 h. Accordingly, DEX inhibited the systemic inflammatory response, but had no direct effect on either testicular steroidogenesis or intra-testicular inflammation, at the dose employed. These data suggest that the inhibition of Leydig cell steroidogenesis at 6h after LPS injection, which was not prevented by co-administration of DEX, is most likely due to direct actions of LPS at the testicular level. In contrast, the later Leydig cell inhibition (at 18 h) may be attributable to extra-testicular effects of LPS, such as increased circulating inflammatorymediators or the release of endogenous glucocorticoids, that were inhibited by DEX treatment. These data indicate that the early and late phases of Leydig cell inhibition following LPS administration are due to separate mechanisms.

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Documento generato il 28/09/20 alle ore 15:36:40