[Effects of triptolide on hypothalamic-pituitary-adrenal axis of rats].
OBJECTIVE
To observe the effects of triptolide on the hypothalamic-pituitary-adrenal axis (HPAA) of rats in light of morphological and functional changes.


METHODS
Thirty Sprague-Dawley (SD) male rats were randomized into 3 groups and given 2% propylene glycol, mixture of propylene glycol and prednisone acetate or compounds of propylene glycol and triptolide by gavage, respectively, for consecutive 7 weeks. Determination in the 3 groups was conducted concerning the contents of blood plasma cortisol (COR), adrenocorticotropic hormone (ACTH) and corticotropin-releasing hormone (CRH) besides measurement of the rats' body weight, coefficient of the adrenal gland and observation of the histopathological changes in fascicular zone of adrenal cortex. Immunohistochemical staining technique was used to detect the expression of ACTH in pituitary in the 3 groups.


RESULTS
(1) The content of COR in the groups of triptolide and prednisone acetate appeared lower and serum ACTH showed no significant difference, but CRH in the group of triptolide was augmented as compared with the control group (P < 0.05). (2) The rats' weight in the groups of triptolide and prednisone acetate was declined, and yet, the coefficient of the adrenal gland remained no significant change in comparison with the controls. HE staining and electron microscopy examination revealed thinned and constricted zona fasciculata in adrenal gland in the rats of triptolide and prednisone acetate, with hypofunction. ACTH expression in the group of triptolide was higher than that of the control group (P < 0.05).


CONCLUSIONS
Morphologically and functionally, the findings suggest that long-term use of triptolide may result in atrophied cortex and hypofunction of the adrenal gland, leading to augmented production and secretion of CRH and ACTH from respective hypothalamic and pituitary.
Zhu
Jian-hua
JH
The Third Medical Department, Wannan Medical College, Wuhu 241002, China.
Hu
Yong-liang
YL
Zhang
Wu
W
Guan
Wei
W
Huang
Guang-zhao
GZ
D000302:Adrenal Cortex / Q000187:drug effects / Q000473:pathology* / Q000503:physiopathology; D000324:Adrenocorticotropic Hormone / Q000097:blood / Q000378:metabolism; D000818:Animals; D003346:Corticotropin-Releasing Hormone / Q000097:blood / Q000378:metabolism; D004224:Diterpenes / Q000009:adverse effects / Q000494:pharmacology*; D004852:Epoxy Compounds / Q000009:adverse effects / Q000494:pharmacology; D006854:Hydrocortisone / Q000097:blood; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects* / Q000503:physiopathology; D007150:Immunohistochemistry; D008297:Male; D010616:Phenanthrenes / Q000009:adverse effects / Q000494:pharmacology*; D010913:Pituitary-Adrenal System / Q000187:drug effects* / Q000503:physiopathology; D011241:Prednisone / Q000008:administration & dosage / Q000494:pharmacology; D019946:Propylene Glycol / Q000008:administration & dosage / Q000494:pharmacology; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley
D004224:Diterpenes; D004852:Epoxy Compounds; D010616:Phenanthrenes; C001899:triptolide; D019946:Propylene Glycol; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone; D011241:Prednisone; D006854:Hydrocortisone