Background: Sjögren syndrome (SS) is a systematic autoimmune disease, on which traditional therapeutic agents show limited effect. More effective agents with longer-lasting and fewer side effects are needed in the clinic. The aim of this study was to investigate the effects of Ganoderma lucindum spores (GLS) on sialoadenitis of nonobese diabetic (NOD) mice.
Methods: Thirty-two female NOD mice were assigned randomly into 4 groups: low-dose GLS-treated (L-GLS) group and high-dose GLS-treated (H-GLS) group, a dexamethasone group, and a normal saline (NS) control group. Stimulated total saliva flow rate (STFR), area of lymphocytic infiltration in submandibular glands and ratios of CD4(+) and CD8(+) T lymphocytes and B lymphocytes in peripheral blood as well as apoptosis of these subsets and serum IgG level were tested after 10 weeks of treatments. Differences among the groups were analyzed by one-way analysis of variance (ANOVA), Student-Newman-Keuls Test (SNK) was used between each two groups and a P < 0.05 was considered statistically significant.
Results: STFR of the high-dose GLS group increased significantly after a 10-week treatment compared with those of the NS control group (P < 0.05). The incidence of sialoadenitis in GLS-treated NOD mice groups showed no significant difference compared with the control group (P > 0.05), but the area of lymphocytic foci in both the H-GLS and L-GLS groups decreased significantly to 50% of the NS control group (P < 0.05); the ratio of CD4(+)/CD8(+) T lymphocytes and apoptosis of B lymphocytes of NOD mice with sialoadenitis were less and apoptosis of CD4(+) and CD8(+) T lymphocytes were significantly increased compared with the control group (P < 0.05). After pretreatment with H-GLS before sialoadenitis onset, the ratio of CD4(+)/CD8(+) T lymphocyte and the serum IgG levels of NOD mice decreased significantly (P < 0.05).
Conclusions: Pretreatment with H-GLS can relieve symptoms of sialoadenitis in NOD mice. GLS has some protective effects on sialoadenitis in NOD mice through increasing STFR and decreasing the area of lymphocytic foci by regulating the ratio of CD4(+)/CD8(+) T and apoptosis of B lymphocytes.