Neuroprotective effect of Launaea taraxacifolia against neuroinflammation, memory loss and neurobehavioral deficit in a rat model of hypertension: biochemical and immunohistochemical approaches
Authors:
- Ademola Adetokunbo OyagbemiAdemola Adetokunbo Oyagbemi
- Fasilat Oluwakemi HassanFasilat Oluwakemi Hassan
- Olamide Elizabeth AdebiyiOlamide Elizabeth Adebiyi
- Kabirat Oluwaseun AdigunKAKabirat Oluwaseun Adigun
- Oluwabusayo Racheal FolarinOluwabusayo Racheal Folarin
- Temitayo Olabisi AjibadeTemitayo Olabisi Ajibade
- Oluwaseun Olanrewaju EsanOluwaseun Olanrewaju Esan
- Temidayo Olutayo OmobowaleTemidayo Olutayo Omobowale
- Olufunke Eunice Ola-DaviesOlufunke Eunice Ola-Davies
- James Olukayode OlopadeJames Olukayode Olopade
- Adebowale Benard SabaAdebowale Benard Saba
- Adeolu Alex AdedapoAdeolu Alex Adedapo
Open Access
- 27 June 2024
- journal article
- Published by Maad Rayan Publishing Company in Journal of Herbmed Pharmacology
- Vol. 13 (3) , 390-398
Abstract
Introduction: Alterations of antioxidant defense, neuroinflammation, and neurodegeneration are common pathological occurrences associated with neurodegenerative diseases. This study evaluated the neuroprotective effect of Launaea taraxacifolia (LT), popularly known as African Wild lettuce, against neuroinflammation, memory loss, and neurobehavioral deficit. Methods: Adult Wistar rats were used following random assignment into groups 1 to 5. Group one was the normal control. Groups four to five received 40 mg/kg Nω-nitro-l-arginine methyl ester (L-NAME). In addition to L-NAME exposure, groups three and four received 100 and 200 mg/kg LT, whereas group five received 10 mg/kg lisinopril. The experiment lasted for five weeks. Markers of oxidative stress, neurobehavioural studies, histology, and immunohistochemistry of glial fibrillary acidic protein (GFAP), ionised calcium-binding adaptor molecule 1 (Iba-1), as well as anti-calbindin for staining astrocytes, microglia, and Purkinje cells were determined. Results: Malondialdehyde (MDA) and protein carbonyl in the L-NAME alone group were heightened compared to those treated with LT. However, treatment with LT significantly reduced neuronal oxidative stress, neuroinflammation, and neurobehavioural changes. Quantitative analysis of immunohistochemical staining revealed heightened glial fibrillary acidic protein (GFAP), ionised calcium-binding adaptor molecule 1 (Iba-1), as well as anti-calbindin as indicated by astrogliosis, microgliosis, and Purkinje cell degeneration in untreated rats. Moreover, the observed ultrastructural anarchy induced by L-NAME was restored in rats treated with LT (P<0.05). Conclusion: Together, the leaf extract of LT can be effective as a neuroprotective drug candidate.Keywords
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