RhCNB Improves Cyclophosphamide-Induced Immunodeficiency in BALB/c Mice. (27th September 2022)

• Record Type: Journal Article
• Authors: Zhong, Wenhua; Huang, Hui; Yang, Zhaoxin; Chang, Penghuan
• Other Names: Wu Xueliang Academic Editor.
• Is Part Of: Evidence-based complementary and alternative medicine. Volume 2022(2022)
• Publication Date: 2022-09-27
• Subjects: Alternative medicine -- Periodicals; 615.505
• DOI: 10.1155/2022/4891399
• Languages: English
• ISSNs: 1741-427X

Abstract

Abstract : Background . This study aims to explore the immunomodulatory effect of rhCNB on mice with cyclophosphamide (CTX)-induced immunodeficiency through TLR4 /MAPK pathway. Methods . BALB/c mice were randomly divided into three groups: a negative control group, an immunosuppression model group, and a rhCNB treatment group. Tail vein injection of cyclophosphamide (40 mg/kg) was used to establish a mouse immunosuppression model. Intraperitoneal injection of rhCNB (20 mg/kg) was administered to the treatment group, whereas equal quantities of normal saline were given to the control group and model group. Perform peripheral blood routine of CD4, CD8, and CD19 lymphocyte subsets and peripheral blood Th1/Th2 cell subsets 24 hours after the last administration. RT-PCR was used to detect mRNA levels of TLR4, P38, JNK, T-bet, and GATA3, the spleen immune organ index was measured, and the histopathological status of the spleen and thymus was observed. Results . The results showed that compared with the control group, WBC, PLT, LYM, NEU, immune organ index, CD4 + /CD8 + and CD19 + subgroup ratio, and peripheral blood Th1/Th2 cell subgroups decreased in the model group. The mRNA levels of TLR4, P38, JNK, T-bet, and GATA3 decreased compared with the model group, while they increased in the treatment group. Conclusions . rhCNB has an immunomodulatory effect by regulating the expression of Th1/Th2 cytokine balance through the TLR4 /MAPK signaling pathway and promoting the differentiation and proliferation of lymphocytes, thereby improving the immune function.