title: Neuroprotective Effect of Compound Anisodine in a Mouse Model with Chronic Ocular Hypertension.
abstract: BACKGROUND
  Compound 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.
  
  
  METHODS
  Female 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.
  
  
  RESULTS
  Mice 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).
  
  
  CONCLUSIONS
  These findings suggest that CA plays an importantly neuroprotective role on RGCs in a mouse model with chronic ocular hypertension.
authors.forename: Wen-Dong
authors.initials: WD
authors.lastname: Liu
authors.forename: Lan-Lan
authors.initials: LL
authors.lastname: Chen
authors.forename: Ce-Ying
authors.initials: CY
authors.lastname: Shen
authors.affiliation: Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University, Beijing Ophthalmology and Visual Sciences Key Laboratory, Beijing 100730, China.
authors.forename: Li-Bin
authors.initials: LB
authors.lastname: Jiang
mesh_terms: D000818:Animals; D002470:Cell Survival / Q000187:drug effects; D005260:Female; D007150:Immunohistochemistry; D007429:Intraocular Pressure / Q000187:drug effects; D051379:Mice; D008810:Mice, Inbred C57BL; D018696:Neuroprotective Agents / Q000494:pharmacology* / Q000627:therapeutic use*; D009798:Ocular Hypertension / Q000188:drug therapy*; D011897:Random Allocation; D012165:Retinal Ganglion Cells / Q000187:drug effects; D012602:Scopolamine Derivatives / Q000494:pharmacology* / Q000627:therapeutic use*
chemical_list: D018696:Neuroprotective Agents; D012602:Scopolamine Derivatives; C012183:anisodine