Immunomodulatory activity of the aqueous extract from rhizome of Smilax glabra in the later phase of adjuvant-induced arthritis in rats

被引:107
作者
Jiang, JY
Xu, Q
机构
[1] Nanjing Univ, State Key Lab Pharmaceut Biotechnol, Sch Life Sci, Nanjing 210093, Peoples R China
[2] China Pharmaceut Univ, Dept Pharmacol Chinese Mat Med, Nanjing 210009, Peoples R China
关键词
Rhizoma Smilacis Glabrae; immunomodulatory activity; adjuvant arthritis; T lymphocytes; macrophages;
D O I
10.1016/S0378-8741(02)00340-9
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Our previous paper has reported that the aqueous extract from Rhizoma Smilacis Glabrae (RSG) remarkably inhibited the primary inflammation of adjuvant arthritis (AA) in rats. In the present study, we further examined the activity of RSG and its mechanism on the secondary inflammation of AA. The administration of RSG (400 and 800 mg/kg) during the later phase significantly inhibited the swelling of the adjuvant-non-injected footpad of AA rats. The lipopolysaccharide-induced production of IL-1, TNF and NO by peritoneal macrophages was significantly reduced. In contrast, the extract significantly recovered the decrease in weight gain of the AA rats and Concanavalin A-induced T lymphocyte proliferation and IL-2 production by their splenocytes, while prednisolone (10 mg/kg) showed a significant aggravation. Furthermore, RSG significantly recovered the picryl chloride-induced delayed-type hypersensitivity to almost normal levels from the higher or lower levels induced by different treatments of cyclophosphamide with a normalization of CD4/CD8 ratio. These results suggest that RSG exhibit an improvement on AA through down-regulating over-activated macrophages and up-regulating the dysfunctional T lymphocytes during the later phase of arthritis. Such characteristics of RSG on AA may be advantageous to the long-term treatment of clinical rheumatoid arthritis. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:53 / 59
页数:7
相关论文
共 31 条
[1]  
[Anonymous], 1979, HDB EXPT PHARM
[2]  
[Anonymous], 1993, CHIN J IMMUNOL
[3]   CYTOKINES AND CYTOKINE INHIBITORS OR ANTAGONISTS IN RHEUMATOID-ARTHRITIS [J].
AREND, WP ;
DAYER, JM .
ARTHRITIS AND RHEUMATISM, 1990, 33 (03) :305-315
[4]  
BAUMGARTNER WA, 1974, P SOC EXP BIOL MED, V145, P625
[5]   THE BIOLOGY OF CACHECTIN/TNF - A PRIMARY MEDIATOR OF THE HOST RESPONSE [J].
BEUTLER, B ;
CERAMI, A .
ANNUAL REVIEW OF IMMUNOLOGY, 1989, 7 :625-655
[6]  
BOGDAN C, 1992, J BIOL CHEM, V267, P23301
[7]   AUTOIMMUNITY TO CHAPERONINS IN THE PATHOGENESIS OF ARTHRITIS AND DIABETES [J].
COHEN, IR .
ANNUAL REVIEW OF IMMUNOLOGY, 1991, 9 :567-589
[8]  
DING AH, 1988, J IMMUNOL, V141, P2407
[9]  
DING AH, 1987, J IMMUNOL, V139, P1971
[10]  
Du ZY, 1998, ACTA PHARMACOL SIN, V19, P257