ABSTRACT
Objective:To evaluate the efficacy and safety of oral anisodine hydrobromide tablets in the treatment of nonarteritic anterior ischemic optic neuropathy (NAION).Methods:A multicenter nonrandomized controlled trial was conducted.A total of 282 acute NAION patients (282 eyes) were recruited from 16 hospitals in China from July 2020 to May 2021.Patients were divided into two groups according to treatment methods, which were control group (124 cases, 124 eyes) receiving regular treatment including citicoline sodium plus Ginkgo biloba leaf liquid extract or Ginkgo biloba leaf extract tablets plus mecobalamin, and experimental group (158 cases, 158 eyes) receiving treatment in control group plus oral anisodine hydrobromide tablets 1 mg, twice daily for 2 to 3 months.Best corrected visual acuity (BCVA), visual field index (VFI), peripapillary retinal nerve fiber layer (pRNFL) and radial peripapillary capillary vessel density (RPC) were assessed at 1, 2, 3, and 6 months after enrollment using the standard decimal visual acuity chart, 750i Humphery visual field analyzer, Cirrus HD-OCT 4000/Cirrus HD-OCT 5000, RTVue-XR optical coherence tomography respectively.The primary outcomes were BCVA and VFI, and the secondary outcomes were pRNFL, RPC, and the side effects during the follow-up.The study adhered to the Declaration of Helsinki.All patients were fully informed about the treatment and purpose of this study and voluntarily signed the informed consent form.The study protocol was approved by Chinese PLA General Hospital (No.S2020-021-01). Results:In all, 242 patients (242 eyes) completed the follow-up of BCVA, and 98 patients (98 eyes) completed the VFI follow-up.In terms of visual function, BCVA and VFI improved significantly over time in the two groups, and BCVA and VFI were better in experimental group than in control group at various follow-up time points (all at P<0.05). In terms of structure, pRNFL gradually decreased in both groups with the extension of treatment, and pRNFL was significanthy thinner in experimental group than in control group at various follow-up time points (all at P<0.05). There was no significant difference in RPC between the two groups at the last follow-up ( P>0.05). There were two cases with side effects and one case was discontinued due to side effects 25 days after enrollment. Conclusions:Oral anisodine hydrobromide can improve visual acuity and visual field in NAION and accelerate the regression of optic disc edema, with good safety.
ABSTRACT
OBJECTIVE:To study the effects of anisodine hydrobromide on cell apoptosis and extracellular signal-regulated pro-tein kinase 1/2 (ERK1/2) phosphorylation (p-ERK1/2) level in brain tissue of model rats with acute cerebral ischemia-reperfusion injury. METHODS:Rats were randomly divided into sham operation group,model group,positive control group(nimodipine 1.0 mg/kg),anisodine hydrobromide high-dose,medium-dose,low-dose,extreme low-dose groups(1.2,0.6,0.3,0.15 mg/kg),8 in each group. Suture method was used to establish the rat models with acute cerebral ischemia-reperfusion injury. Rats were intrave-nously injected once in tail at 2nd of ischemia and 6th of reperfusion. Then adenosine triphosphate (ATP) enzyme activity,Ca2+content,cell apoptosis in brain tissue,p-ERK1/2 protein expression in brain tissue,and p-ERK1/2/total ERK1/2 (t-ERK1/2) pro-portion in brain tissue of rats were detected after 22 h of reperfusion. RESULTS:Compared with sham operation group,ATP en-zyme activity in brain tissue of rats in model group was obviously decreased,Ca2+ content was obviously increased,density of cell apoptosis in brain tissue was obviously increased,with statistical significances(P<0.01). Compared with model group,density of cell apoptosis in brain tissue was obviously decreased in each administration group;Ca2+ contents in brain tissue of rats in positive control group,anisodine hydrobromide high-dose,low-dose groups were obviously decreased;and p-ERK1/2/t-ERK1/2 proportion in brain tissue of rats in anisodine hydrobromide high-dose,low-dose,extreme low-dose groups were obviously increased,with sta-tistical significances(P<0.05 or P<0.01);the other differences were not statistically significant(P>0.05). CONCLUSIONS:An-isodine hydrobromide can inhibit the cell apoptosis in brain tissue of model rats with acute cerebral ischemia-reperfusion injury,andthe mechanism may be related with activating ERK1/2 signal pathway and regulating ATP enzyme activity to decrease the Ca2+content in the brain tissue.
ABSTRACT
OBJECTIVE:To study the effects of anisodine hydrobromide on cell apoptosis and extracellular signal-regulated pro-tein kinase 1/2 (ERK1/2) phosphorylation (p-ERK1/2) level in brain tissue of model rats with acute cerebral ischemia-reperfusion injury. METHODS:Rats were randomly divided into sham operation group,model group,positive control group(nimodipine 1.0 mg/kg),anisodine hydrobromide high-dose,medium-dose,low-dose,extreme low-dose groups(1.2,0.6,0.3,0.15 mg/kg),8 in each group. Suture method was used to establish the rat models with acute cerebral ischemia-reperfusion injury. Rats were intrave-nously injected once in tail at 2nd of ischemia and 6th of reperfusion. Then adenosine triphosphate (ATP) enzyme activity,Ca2+content,cell apoptosis in brain tissue,p-ERK1/2 protein expression in brain tissue,and p-ERK1/2/total ERK1/2 (t-ERK1/2) pro-portion in brain tissue of rats were detected after 22 h of reperfusion. RESULTS:Compared with sham operation group,ATP en-zyme activity in brain tissue of rats in model group was obviously decreased,Ca2+ content was obviously increased,density of cell apoptosis in brain tissue was obviously increased,with statistical significances(P<0.01). Compared with model group,density of cell apoptosis in brain tissue was obviously decreased in each administration group;Ca2+ contents in brain tissue of rats in positive control group,anisodine hydrobromide high-dose,low-dose groups were obviously decreased;and p-ERK1/2/t-ERK1/2 proportion in brain tissue of rats in anisodine hydrobromide high-dose,low-dose,extreme low-dose groups were obviously increased,with sta-tistical significances(P<0.05 or P<0.01);the other differences were not statistically significant(P>0.05). CONCLUSIONS:An-isodine hydrobromide can inhibit the cell apoptosis in brain tissue of model rats with acute cerebral ischemia-reperfusion injury,andthe mechanism may be related with activating ERK1/2 signal pathway and regulating ATP enzyme activity to decrease the Ca2+content in the brain tissue.
ABSTRACT
Objective To explore the anisodine hydrobromide injection on postoperative visual function recovery in patients with glaucoma.Methods Used retrospective analysis method, 18 cases, 25 eyes glaucoma patients from October 2012 to October 2015 in our hospital undergoing surgery treatment were randomly selected and their clinical data were analyzed.The patients received anisodine hydrobromide injection postoperative,and intraocular pressure andvision correction were compared before and after treatment.Results After treatment,the patient’ s average intraocular pressure was(13.64 ±2.35)mmHg,which was signigicantly lower than(36.68 ±3.56)mmHg before treatment(P <0.05);postoperative follow-up,vision correction of 14 cases(21 eyes) was above 0.3,accounted for 84%,which was statistically significant compared with the preoperative (P<0.05);there were 3 cases(4 eyes)of postoperative complications,including one eye with corneal edema,1 eye with anterior chamber bleeding,2 eyes for fiber exudative inflammation, the complication rate was 16%.Conclusion Postoperative patients with compound anisodine hydrobromide injection adjuvant therapy has significant clinical effect, not only could significantly improve the patient ’ s visual function, and reduce incidence of postoperative complications with high security.