ArticleChinese medical journal2015
Neuroprotective Effect of Compound Anisodine in a Mouse Model with Chronic Ocular Hypertension.
Article in Chinese medical journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Efficacy and safety of anisodine hydrobromide injection in acute ischemic stroke-a multicenter real-world observational study.Frontiers in pharmacology · 2026Trial
- Anisodine hydrobromide targets matk and prevents delayed rtPA thrombolysis-induced vasogenic cerebral edema in ischemic stroke.Nature communications · 2026Article
- Review
- Sequential bilateral retinal artery occlusions with promising visual prognosis in a diabetic patient: a case report and literature review.BMC ophthalmology · 2025Review
- Unilateral branch retinal vein occlusion and contralateral branch retinal artery occlusion: a case report and comprehensive literature review.Frontiers in medicine · 2025Article
- Effects of Anisodine Hydrobromide on the Cardiovascular and Respiratory Functions in Conscious Dogs.Drug design, development and therapy · 2020Article
- Compound anisodine affects the proliferation and calcium overload of hypoxia-induced rat retinal progenitor cells and brain neural stem cells via the p-ERK1/2/HIF-1α/VEGF pathway.Experimental and therapeutic medicine · 2017Article
- Observation on therapeutic efficacy of rt-PA intravenous thrombolysis combined with compound anisodine injection on central retinal artery occlusion.Experimental and therapeutic medicine · 2016Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCompound anisodine (CA) is a compound preparation made from hydrobromide anisodine and procaine hydrochloride. The former is an M-choline receptor blocker with the function of regulating the vegetative nervous system, improving microcirculation, and so on. The latter is an antioxidant with the activities of neuroprotection. This study aimed to investigate the potential neuroprotection of CA, which affects the degeneration of the retinal ganglion cells (RGCs) in an animal model with chronic ocular hypertension.
methodsFemale C57BL/6J mice (n = 24) were divided randomly into four groups: normal control group without any treatment (Group A, n = 6); CA control group with feeding the CA solution (Group B, n = 6); microbeads (MBs) control group with injecting MB into the anterior chamber (Group C, n = 6); CA study group with MB injection and with feeding the CA solution (Group D, n = 6). Intraocular pressure (IOP) was measured every 3 days after MB injection. At the 21st day, neurons were retrograde-labeled by Fluoro-Gold (FG). Animals were sacrificed on the 27th day. Retinal flat mounts were stained immunohistologically by α2-III-tubulin. FG-retrograde-labeled RGCs, α2-III-tubulin-positive RGCs, and α2-III-tubulin-positive nerve fibers were quantified.
resultsMice of Groups C and D expressed the incidence of consistent IOP elevation, which is above the IOP level of Group A with the normal one. There is no significant difference in IOP between Groups A and B (P > 0.05). On the 27th day, there were distinct loss in stained RGCs and nerve fibers from Groups C and D compared with Group A (allP < 0.001). The quantity was significantly higher in Group D as compared to Group C (allP < 0.001) but lower than Group A (allP > 0.001). There was no significant difference in the quantity of RGCs and nerve fibers between Groups A and B (allP > 0.05).
conclusionsThese findings suggest that CA plays an importantly neuroprotective role on RGCs in a mouse model with chronic ocular hypertension.
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