Memory is an essential aspect of human cognition. A decrease in this aspect is well associated with Alzheimer’s disease (AD). The development of a novel cognitive enhancer (CE) may help overcome AD-related problems. In this study, we evaluated the CE effect of Caesalpinia sappan L. (CS) in memory deficit mice. Administration of its ethanolic extract (250 and 500 mg/kg body weight (BW)) and brazilin (5 and 10 mg/kg BW) ameliorated the scopolamine-amnesic effect, as evidenced by significant decreases (p < 0.01, p < 0.05) in the escape latency time and increases (p < 0.01) in the percentage of time spent in the target quadrant of the Morris water maze test. We also examined the cyclic adenosine monophosphate (cAMP) level, protein kinase A (PKA) activity, and protein expression levels of phosphorylated cAMP response element binding (pCREB) and brain-derived neurotrophic factor (BDNF) in hippocampal tissues to elucidate the underlying molecular mechanism. Results showed that CS wood ethanolic extract and brazilin not only significantly increase (p < 0.01, p < 0.05) cAMP levels and PKA activity but also significantly enhance (p < 0.01, p < 0.05) the expression level of pCREB and BDNF in the hippocampus. These findings indicate that CS activates the cAMP/PKA/CREB/BDNF pathway. Taken together, our results demonstrate that CS is a promising herb that could be developed as a CE agent.
Cisplatin is widely used for the chemotherapy of head and neck cancer. However, it has a significant ototoxicity. Nigella sativa has been scientifically proven to have numerous benefits included to prevent adverse effect of a drug. This literature review aimed to evaluate the protective role of N. sativa oil against cisplatin-induced ototoxicity. Relevant publications were searched from PubMed and Google Scholar databases within the last 10 years. Ototoxicity due to cisplatin can occur through the intrinsic and extrinsic pathways. Cisplatin causes endoplasmic reticulum stress, DNA damage, increased reactive oxygen species (ROS) and inflammatory processes, resulting in increased apoptosis of cochlear outer hair cells. The active constituents of N. sativa including flavonoids, phenolics and thymoquinone can prevent the cisplatin-induced ototoxicity. Examination of endogenous antioxidants, antiapoptotic, and proinflammatory could be used as primary approach to evaluate the protective role of N. sativa against cisplatin-induced ototoxicity.
Cognitive impairment (CI) is a highly complex central nervous system disorder commonly associated with aging. This condition is characterized by a progressive reduction of cognitive function. Modern synthetic drugs have been granted clinical approval for the treatment of CI. However, most of these drugs show insufficient efficacy and undesired side effects in clinical practice. Alternative drugs for CI are required to overcome these problems. Medicinal plants and their bioactive molecules remain the main sources for new drug discovery, and they have the potential to be developed as novel drugs for CI. Many reports have demonstrated the activity of other medicinal plants and their active metabolites for CI in various experiments. In this article, we summarize the potency of plant natural compounds for CI, focusing on cognitive-enhancing activity in amnesic-animal experimental models. We also discuss the pathophysiological basis of CI and propose potential therapeutic targets of CI using plant natural compounds. Additionally, we highlight promising natural compounds for CI and discuss their possible mechanisms of action. This review provides insight into the effort of discovery and development of pharmaceutical agents derived from medicinal plants to combat CI.
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