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Medicinal Potential of Fenugreek in Neuropathy and Neuroinflammation Associated Disorders
Published in Dilip Ghosh, Prasad Thakurdesai, Fenugreek, 2022
Aman Upaganlawar, Chandrashekhar Upasani, Mayur B. Kale
Neuroinflammation is a complex response to various mediators, pro-inflammatory molecules, and reactive oxygen species leading to tissue damage. Neuroinflammation is a prominent pathological feature of neurological disorders, characterized by activated microglia and infiltrating T-lymphocytes at neuronal injury (Skaper et al. 2018). In response to alterations induced in the innate immune system, T-lymphocytes, members of the adaptive immune system, infiltrate the CNS at sites of neuronal injury. Thus, active participation of inflammation in neurological disease pathogenesis and its contribution to the neurodegenerative pathology and tissue destruction is evident (Simon, Obst, and Gomez-Nicola 2019).
Traditional Malay Ulam for Healthy Ageing
Published in Goh Cheng Soon, Gerard Bodeker, Kishan Kariippanon, Healthy Ageing in Asia, 2022
Jamia Azdina Jamal, Khairana Husain
Puttarak et al. (2017) performed a systematic review and meta-analysis of the effect of Centella asiatica on cognitive abilities. A quantitative synthesis of 11 related papers found no conclusive evidence to support the effect of C. asiatica on overall cognitive performance improvement. However, C. asiatica could improve working memory. When mixed with other herbs, it could improve attentiveness and focus, executive functioning skills and information processing speed. In vitro and in vivo studies conducted by Hafiz et al. (2020) have reported that an ethanol extract (95%) of C. asiatica inhibits acetylcholinesterase, LPS-induced neuroinflammation and oxidative stress. Neuroinflammation is associated with neurodegenerative diseases such as Alzheimer’s disease (AD) and cognitive dysfunction. Agathisflavone isolated from 80% methanol extract of Anacardium occidentale leaves inhibits neuroinflammation in BV2 microglia via activation of immune-related NF-κB signalling pathway (Velagapudi et al. 2018).
Spinal Cord Disease
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
The mechanisms involved in motor neuron cell survival and death are not well known. It is suspected that cellular mechanisms are at play in the motor neuron degeneration: Excitotoxicity via overstimulation of postsynaptic glutamate receptors.Oxidative stress.Protein and neurofilament aggregation.Disordered axonal transport and cellular signaling mechanisms.Neuroinflammation, although clinical trials of immunomodulating therapies have failed to impact the clinical course of the disease.
Anti-neuroinflammatory effects of alkaloid-enriched extract from Huperzia serrata on lipopolysaccharide-stimulated BV-2 microglial cells
Published in Pharmaceutical Biology, 2023
Thu Kim Dang, Seong-Min Hong, Vui Thi Dao, Phuong Thi Thu Tran, Hiep Tuan Tran, Giang Hoang Do, Thanh Nguyen Hai, Hang Thi Nguyet Pham, Sun Yeou Kim
Neuroinflammation is an inflammatory process involved in normal brain function that leads to neurodegeneration due to the innate and adaptive immune systems in the brain. Inflammation associated with AD progression may be induced by different cytokines and ILs (Calsolaro and Edison 2016). Microglia are the first and foremost form of active immune defense in the CNS. In the pathological condition of neuroinflammation, microglial cells are stimulated and their morphology changes. It triggers the release of inflammatory mediators, such as chemokines, cytokines, and cytotoxic molecules (such as COX-2, glutamate, and prostaglandins). Microglia can activate intracellular downstream signaling pathways involving MAPKs (Dragic et al. 2021). Extracellular stimuli, such as LPS, a component of gram-negative bacteria, can activate microglia and secrete pro-inflammatory mediators, such as NO, PGE2, IL-1β, IL-6, and TNF-α, which initiate several major cellular responses that contribute to the pathogenesis of neuroinflammation (Batista et al. 2019). Therefore, interventions to inhibit the production of these mediators are a promising approach for the prevention or treatment of neuroinflammation.
Protective effects of Centella asiatica extract on spatial memory and learning deficits in animal model of systemic inflammation induced by lipopolysaccharide
Published in Annals of Medicine, 2023
Mazura Md Pisar, Beng Jin Chee, Idris Long, Asiah Osman
It has been postulated that neuroinflammation plays a role in cognitive impairment and degenerative illnesses of the nervous system. Preceding studies have reported that chronic neuroinflammation elicited by systemic inflammation of LPS has been implicated in the persistent discriminative deficits of hippocampal-dependent tasks of location memory which is known to be impaired with aging process [16–19]. The present study showed that LPS group of animal displayed learning and memory impairment which correlate with a deficit in learning ability and reference memory which are attributed to Alzheimer’s-like cognitive dysfunction. This finding is in line with a study by Bossu and colleague [19] that demonstrated a single dose of LPS was able to evoke persistent cognitive impairment characterized by noticeable deficiencies in reacting to environment modifications which could be due to reduced motivational or attentional deficits. Hence, this model may represent a viable option for the investigation of Alzheimer’s-related diseases and the screening of therapeutic agents. By using Morris Water Maze (MWM) test, this study demonstrates the cognitive performance improvements of CA extract following systemic inflammation induced by LPS.
Oleanolic acid and ursolic acid: therapeutic potential in neurodegenerative diseases, neuropsychiatric diseases and other brain disorders
Published in Nutritional Neuroscience, 2023
Chen Chen, Qidi Ai, Axi Shi, Nan Wang, Lina Wang, Yuhui Wei
Under normal physiological conditions, neuroinflammation contributes to repair of nervous system damage, and when the inflammatory response is excessive, it will cause cell damage. Neuroinflammation is a common symptom in brain disorders. OA shows anti-inflammatory effects in neurodegenerative diseases including AD [20], PD [35,36], and MS [42]. UA also has anti-inflammatory effects in AD [26], PD [39], and MS [48]. The effects of OA [78] and UA [74] on reducing the damage of IS and SAH are also related to anti-inflammation. In addition, the anti-aging effect of UA is also associated with anti-inflammation [92], and both OA [91] and UA [90] can improve cognitive deficits through anti-neuroinflammation. A recent review has summarize the neuroprotective effects of UA on several neurological diseases focus on antioxidant and anti-inflammatory point of view [86], and can be can be consulted.