1.Compound anisodine and physical therapy treat child amblyopia:report of 300 cases
Mengting LU ; Yongxian TAO ; Pinghua LI ; Bo TU
Journal of Third Military Medical University 2003;0(19):-
Objective To investigate the combination of compound anisodine and physical therapy in the treatment of amblyopia,and its possible mechanism.Methods Totally 300 outpatients with amblyopia(3 to 14 years old) were randomly and equally divided into treatment group and control group.In the treatment group,subcutaneous injection of compound anisodine(2 ml,once per day) to the superficial temporal artery of eye was given for a course of 14 d and followed by another course after 5 days'interval.Cover treatment was carried out at the same time.The control group was only treated with physical therapy.Vision,central retinal artery peak systolic velocity(PSV) and diastolic resistance index(RI) were measured during the 3 months' follow-up.Results The 3 to 6-year-old efficiency was 75.0%,7 to 9-year-old efficiency was 69.6%,and 10 to 14-year-old efficiency was 61.1% ;The difference of efficiency between therapy group and control group was very significant(P0.05).Conclusion Compound anisodine plus physical therapy for amblyopia at different ages and varying degrees are effective and safe.The mechanism may be due to enhanced retinal blood supply.
2.Berberine Inhibits Atherosclerosis by Regulating Lipophagy Via Targeting Wnt5a/NPC1 Signaling Pathway
Caiyun YANG ; Qiwen LU ; Sang LUO ; Mengting TU ; Tong ZHAO ; Cuicui ZHENG ; Qiang WAN
Chinese Journal of Experimental Traditional Medical Formulae 2023;29(18):62-68
ObjectiveTo investigate the regulatory effect and molecular mechanism of berberine (BBR) on lipophagy in the prevention and treatment of atherosclerotic (AS) lesions in mice. MethodFifty apolipoprotein E-knockout (ApoE-/-) mice were randomly divided into an AS model group, an atorvastatin group (5 mg·kg-1), and low-, medium-, and high-dose BBR groups (2.5, 5, 10 mg·kg-1). Ten C57BL/6J mice were assigned to the control group. After 12 weeks, hematoxylin-eosin (HE) and oil red O staining were performed to assess the histopathological changes of AS plaques in the aorta. Biochemical analysis was used to measure serum lipid levels, and enzyme-linked immunosorbent assay (ELISA) was employed to measure the levels of inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), oxidative stress marker reactive oxygen species (ROS), and serum lipophagy marker Beclin1 and microtubule-associated protein 1 light chain 3 Ⅱ (LC3Ⅱ). The xanthine oxidase method was used to measure serum superoxide dismutase (SOD) activity. Immunohistochemistry (IHC) was used to detect the distribution of wingless-type MMTV integration site family member 5a (Wnt5a) and Nieman Pick type C1 (NPC1) in the aorta, and Western blot was used to determine the protein expression of Wnt5a and NPC1 in the aorta. ResultCompared with the control group, the AS model group showed significant AS plaque formation, significantly elevated levels of serum total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), IL-6, TNF-α, and ROS, aortic Wnt5a distribution and protein expression (P<0.01), and significantly reduced levels of serum high-density lipoprotein cholesterol (HDL-C), SOD, Beclin1, LC3Ⅱ, and aortic NPC1 distribution and protein expression (P<0.01). Compared with the AS model group, the atorvastatin group, and high- and medium-dose BBR groups showed a significant reduction in AS plaque area (P<0.05, P<0.01), significantly decreased levels of serum TC, TG, LDL-C, IL-6, TNF-α, ROS, and aortic Wnt5a distribution and protein expression (P<0.05, P<0.01), and significantly increased levels of serum HDL-C, SOD, Beclin1, LC3Ⅱ, and aortic NPC1 distribution and protein expression (P<0.05, P<0.01). There was no statistically significant difference in the above indicators between the atorvastatin group and the medium-dose BBR group. ConclusionBBR can competitively bind to Wnt5a to activate NPC1 expression, upregulate lipophagy levels, reduce blood lipids, and inhibit the release of inflammatory mediators and oxidative stress damage, thereby exerting a preventive and therapeutic effect on AS.