Table 1.
Disease | Animal Model | Treatment | Tissue Sample | Result | References |
---|---|---|---|---|---|
AD | 48 male albino rats | Lipopolysaccharide with a dose of 0.8 mg/kg was given as an injection into the peritoneum for one dose. Group III was treated by a TQ 10 mg/kg injection into the peritoneum. Group IV was treated by PNU-120596 1 mg/kg injection into the peritoneum. | frontal lobe | More effective using TQ or α7 nAChR agonist and PAM. | [1] |
AD | Male rats | D-gal dose of (60 mg/kg day) and AlCl3 dose of (10 mg/kg day) administered through the peritoneum (i.p.) once daily for 42 days, and after 4 weeks, TQ was administered intragastrically (i.g.) as a dose of (20 mg/kg/day) once daily for 14 days. | whole brain | Increased potential protective effect of TQ. | [2] |
AD | Twelve-week-old male Wistar rats | Group (1) is the Control group received (saline). group (2) received LPS (1 mg/kg i.p.), groups (3–5) received 2, 5, or 10 mg/kg TQ treatment. | hippocampal and cortical tissues | Improved the impairment of learning and memory. | [33] |
AD | Amyloid beta- (Aβ-) induced neurotoxicity | The intervention group received Aβ1–42 and TQ as a treatment simultaneously for 72 h. | hippocampal and cortical neurons | Efficient attenuation of Aβ1–42-induced neurotoxicity | [47] |
AD | Adult female rats injected by STZ (3 mg/kg) |
TQ dose of 20 mg/kg/day was given to rats for 15 days; on the 15th day, STZ injection was given. | hippocampus | Noticeable decrease in STZ-induced neurodegeneration. | [48] |
AD | Thirty adult male Sprague Dawley albino rats | (Control group, Group 2 is people with AD): induced by oral AlCl3 (17 mg/kg/day) for 4 weeks. Group 3 (TQ/AD): treated with oral TQ (10 mg/kg/day) and AlCl3 (17 mg/kg/day) for period of 4 weeks. | hippocampus | Protective effects against neurodegeneration. | [49] |
AD | Adult female rats injected with aggregated Aβ1–42 |
TQ dosage of (10 mg/kg) was given. The other group received a TQ dose of 20 mg/kg) for 15 days. | hippocampal tissue | Reduced neurotoxicity by removing Aβ plaques and restoring neuron viability. | [50] |