TY - BOOK AU - Merhan Ossama Abdelghany Hindam AU - Nesrine S. Elsayed , AU - Rabab Hamed Sayed , TI - Possible neuroprotective effects of the coumarins : : Xanthotoxin and umbelliferone in the model of streptozotocin-induced sporadic Alzheimer{u2019}s disease in rats / PY - 2021/// CY - Cairo : PB - Merhan Ossama Abdelghany Hindam , KW - Alzheimer's disease KW - Umbelliferone KW - Xanthotoxin N1 - Thesis (M.Sc.) - Cairo University - Faculty of Pharmacy - Department of Pharmacology and Toxicology; Issued also as CD N2 - The aim of the present study was to assess the neuroprotective effects of xanthotoxin and umbelliferone in streptozotocin (STZ)-induced cognitive dysfunction in rats. Animals were injected intracerebroventricularly (ICV) with STZ (3 mg/kg) once to induce a sporadic Alzheimer's disease (SAD)-like condition. Xanthotoxin or umbelliferone (15 mg/kg, i.p.) were administered 5 hr after ICV-STZ and daily for 20 consecutive days. Xanthotoxin or umbelliferone prevented cognitive deficits in the Morris water maze and object recognition tests. In parallel, xanthotoxin or umbelliferone reduced hippocampal acetylcholinestrase activity and malondialdehyde level. Moreover, xanthotoxin or umbelliferone increased glutathione content. These coumarins also modulated neuronal cell death by reducing the level of proinflammatory cytokines) tumour necrosis factor-alpha and interleukin-6), inhibiting the overexpression of inflammatory markers (nuclear factor mB [NF-mB] and cyclooxygenase II), and upregulating the expression of NF-mB inhibitor (ImB-Ü). Interestingly, xanthotoxin diminished phosphorylated JAK2 and phosphorylated STAT3 protein expression, while umbelliferone markedly replenished nuclear factor erythroid-derived 2-like 2 (Nrf2) and haem oxygenase-1 (HO-1) levels. The current study provides evidence for the protective effect of xanthotoxin and umbelliferone in STZ-induced cognitive dysfunction in rats. This effect may be attributed, at least in part, to inhibiting acetylcholinestrase and attenuating oxidative stress, neuroinflammation and neuronal loss. UR - http://172.23.153.220/th.pdf ER -