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Activation of the nerve growth factor (NGF) signaling pathway is a potential method of treatment for retinal ganglion cell (RGC) loss due to traumatic optic neuropathy (TON). The present study aimed to explore the biological effects of injecting Astragalus membranaceus (A. mem) on RGCs in an experimental TON model. Adult male Wistar rats were randomly divided into three groups: sham-operated (SL), model (ML), and A. mem injection (AL). The left eyes of the rats were considered the experimental eyes, and the right eyes served as the controls. AL rats received daily intraperitoneal injections of A. mem (3 mL/kg), whereas ML and SL rats were administered the same volume of normal saline. The TON rat model was induced by optic nerve (ON) transverse quantitative traction. After two-week administration, the number of RGCs was determined using retrograde labeling with Fluoro-Gold. The protein levels of NGF, tyrosine kinase receptor A (TrkA), c-Jun N-terminal protein kinase (JNK), JNK phosphorylation (p-JNK), and nuclear factor kappa-B (NF-κB) were assessed using western blotting. The levels of p75 neurotrophin receptor (p75NTR) and NF-κB DNA binding were examined using real-time PCR and an electrophoretic mobility shift assay. In addition, the concentrations of JNK and p-JNK were assessed using an enzyme-linked immunosorbent assay. Results. The number of RGCs in ML was found to be significantly decreased P < 0.01 relative to both AL and SL, together with the downregulation of NGF P < 0.01 , TrkA P < 0.05 , and NF-κB P < 0.01 ; upregulation of p75NTR mRNA P < 0.01 ; and increased protein levels of JNK P < 0.05 and p-JNK P < 0.05 . Treatment using A. mem injection significantly preserved the density of RGCs in rats with experimental TON and markedly upregulated the proteins of NGF P < 0.01 , TrkA P < 0.05 , and NF-κB P < 0.01 and downregulated the mRNA level of p75NTR P < 0.01 , as well as the proteins of JNK P < 0.05 and p-JNK P < 0.01 . Thus, A. mem injection could reduce RGC death in TON induced by ON transverse quantitative traction by stimulating the NGF signaling pathway.
Activation of the nerve growth factor (NGF) signaling pathway is a potential method of treatment for retinal ganglion cell (RGC) loss due to traumatic optic neuropathy (TON). The present study aimed to explore the biological effects of injecting Astragalus membranaceus (A. mem) on RGCs in an experimental TON model. Adult male Wistar rats were randomly divided into three groups: sham-operated (SL), model (ML), and A. mem injection (AL). The left eyes of the rats were considered the experimental eyes, and the right eyes served as the controls. AL rats received daily intraperitoneal injections of A. mem (3 mL/kg), whereas ML and SL rats were administered the same volume of normal saline. The TON rat model was induced by optic nerve (ON) transverse quantitative traction. After two-week administration, the number of RGCs was determined using retrograde labeling with Fluoro-Gold. The protein levels of NGF, tyrosine kinase receptor A (TrkA), c-Jun N-terminal protein kinase (JNK), JNK phosphorylation (p-JNK), and nuclear factor kappa-B (NF-κB) were assessed using western blotting. The levels of p75 neurotrophin receptor (p75NTR) and NF-κB DNA binding were examined using real-time PCR and an electrophoretic mobility shift assay. In addition, the concentrations of JNK and p-JNK were assessed using an enzyme-linked immunosorbent assay. Results. The number of RGCs in ML was found to be significantly decreased P < 0.01 relative to both AL and SL, together with the downregulation of NGF P < 0.01 , TrkA P < 0.05 , and NF-κB P < 0.01 ; upregulation of p75NTR mRNA P < 0.01 ; and increased protein levels of JNK P < 0.05 and p-JNK P < 0.05 . Treatment using A. mem injection significantly preserved the density of RGCs in rats with experimental TON and markedly upregulated the proteins of NGF P < 0.01 , TrkA P < 0.05 , and NF-κB P < 0.01 and downregulated the mRNA level of p75NTR P < 0.01 , as well as the proteins of JNK P < 0.05 and p-JNK P < 0.01 . Thus, A. mem injection could reduce RGC death in TON induced by ON transverse quantitative traction by stimulating the NGF signaling pathway.
This study investigated the effects of Astragalus complanatus flavonoids on immune function and liver fibrosis in alcohol-induced liver rats. 80 healthy ACL female rats were grouped as healthy group, alcohol liver group (AL group), low-dose group (30 mg/kg) (LD group), and high-dose group (120 mg/kg) (HD group). ALT and AST were measured by CD4+ and CD8+ were measured by flow cytometry. Radioimmunoassay measured HA, LN, PC-III, and IV-c, while Western blot measured TNF-α/TLR4/MYD88/NF-kB. The liver cells from healthy group were neatly arranged with clear boundaries, disordered in the alcohol liver group with blurred lobules, with a large number of vacuoles and inflammatory cell infiltrations. The liver cells from 2 intervention groups were relatively clearly arranged and intracellular vacuoles were reduced. The ALT and AST levels in AL group were highest than healthy group (P < 0.05), followed by LD (P < 0.05) and HD group (P < 0.05). Compared with healthy group, the CD4+ and CD4+/CD8+ content in the AL group decreased and CD8+ increased (P < 0.05). In comparison with AL group, CD4+ and CD4+/CD8+ level increased and CD8+ decreased (P < 0.05) in LD and HD group with increased HD group (P < 0.05). The expressions of HA, LN, PC-III, IV-c, TNF-α, TLR4, MYD88, and NF-kB in healthy group were lower than AL group (P < 0.05) and lowly expressed in AL group and highly expressed in HD group (P < 0.05). The flavonoids of Astragalus complanatus can therefore reduce the degree of liver fibrosis in alcohol-induced rats and improve the immunity of rats by inhibiting cytokines in the TNF-α signaling pathway (Fig. 1).
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