Objective:The objective of this study is to investigate the inhibitory effect of LXHY,a Chinese medicine compound formula,on choroidal neovascularization(CNV) and to find the possible working mechanism.Methods:CNV was induced in C57 BL/6 mice by krypton laser and bone marrow-derived cells(BMCs) isolated from enhanced green fluorescent protein(EGFP) transgenic mice were injected through tail vein 0.5–1 h after the laser surgery.The BMC-treated mice were randomly divided into two groups gavaged with either distilled water(DW group) or LXHY formula solution from day 1 after laser surgery.On days 7,14,and 28 after treatment,histopathologic examination,fundus fluorescein angiography,and choroidal flatmount assay were performed to measure the CNV severity and BMC recruitment.CXCR4 levels in peripheral blood were measured by enzyme-linked immunosorbent assay.Stromal cell-derived factor-1α(SDF?1α),vascular cell adhesion molecule-1(VCAM-1),and intercellular adhesion molecule-1(ICAM-1) were detected by immunofluorescent staining.Results:On days 7 and 14 after treatment,CNV lesions in the LXHY-treated mice showed less recruitment of BMCs and were smaller in size compared to DW-treated mice.Histological examination also confirmed less severe CNV lesions in the LXHY group.CXCR4 levels in peripheral blood in the LXHY group were less than that of DW group on days 7 and 14.Moreover,the expression levels of SDF-1α,ICAM?1,and VCAM?1 at the lesion sites in the LXHY group were lower compared with the DW group.Conclusion:This experiment indicated that LXHY formula could inhibit CNV formation and development,probably by inhibiting the recruitment and attachment of BMCs into CNV area.
Objective: To observe the contribution of Borneolum syntheticum to the intervention effect of Liuwei Dihuang Pill(六味地黄丸, LDP) on experimental retinal degeneration, and initially investigate the mechanism of Borneolum syntheticum as meridian-lead-in drug. Methods: A total of 180 sodium iodateinduced retinital degeneration rats were randomly divided into three groups, including distilled water group, LDP group, and LDP+Borneolum syntheticum(LDP+BS) group. Twenty normal rats were fed regularly without any treatment as normal control. On day 7 and 14 after treatment, histopathological study and transferase-mediated deoxyuridine triphosphate-biotin nick end labeling(TUNEL) test were performed to evaluate the retinopathy. Claudin-5 expression at blood-retina barrier(BRB) was detected by Western blot at different time points from 0.5 to 8 h after gavage. Results: On day 7 and 14 after treatment, the retinal lesion grades were significantly different among the three groups(P<0.05). The grade in the LDP+BS group was significantly less than the LDP and distilled water groups(both P<0.05), no significant difference was observed between the LDP and distilled water groups(P>0.05). The apoptosis rates in the LDP+BS group was significantly less than the distilled water and LDP groups(both P<0.05), while there was no significant difference between LDP and distilled water groups(P>0.05). Expression of claudin-5 in LDP+BS group was significantly less than the other two groups at 0.5, 1 and 2 h after gavage(P<0.05). There was no apparent difference among the three groups at 4 and 8 h after gavage(P>0.05). Conclusion: Borneolum syntheticum could strengthen the effect of LDP on experimental retinal degeneration, indicated that Borneolum syntheticum might play the role of meridian-lead-in drug in the formula. The mechanism may be due to Borneolum syntheticum could promote the physiologically openness of bloodretina barrier through transiently affecting the expression of claudin-5.
