Journal of the American Nutrition Association · 2026
Efficacy of a Terminalia chebula-Boswellia serrata Combination in Lipopolysaccharide-Induced Neuroinflammation in Sprague Dawley Rats.
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Yadav Pramod Kumar, Kavungala Krishna Chaitanya, Park Geum Duck, Kim Kyung Seok, Kim Dahee, Kundimi Sreenath, Alluri Krishnaraju Venkata, Sengupta Krishanu, Bagchi Debasis
Аннотация
OBJECTIVE: To evaluate the efficacy of a standardized formulation of Terminalia chebula and Boswellia serrata (LN19184) against lipopolysaccharide (LPS)-induced neuroinflammation and associated neurodegenerative markers in in vitro and in vivo models.
METHODS: The antioxidant and acetylcholinesterase (AChE) inhibitory activities of LN19184 were assessed and compared with those of the individual plant extracts. Acetylcholine (ACh) levels were measured in SH-SY5Y neuronal cells. In LPS-stimulated cells, the effects of LN19184 on nuclear factor kappa B (NF-κB) phosphorylation, Tau phosphorylation, and β-secretase 1 (BACE-1) expression were evaluated. In vivo, Sprague Dawley rats were challenged with LPS and treated with LN19184. Behavioral assessments of spatial learning, working memory, and recognition memory were conducted. Hippocampal oxidative stress, inflammatory markers, apoptosis-related proteins, and neurodegenerative or synaptic plasticity-associated proteins were analyzed.
RESULTS: LN19184 exhibited greater (p < 0.05) superoxide anion scavenging and AChE inhibitory activities than the individual extracts and increased ACh levels in SH-SY5Y cells. In LPS-stimulated cells, LN19184 significantly reduced NF-κB phosphorylation, Tau phosphorylation, and BACE-1 expression (p < 0.05). In LPS-challenged rats, LN19184 significantly improved spatial learning, working memory, and recognition memory compared with the LPS control group (p < 0.05). These behavioral benefits were accompanied by reduced hippocampal oxidative stress and lower levels of inflammatory markers. LN19184 supplementation increased hippocampal B-cell lymphoma 2 (Bcl-2) and reduced caspase-3 and Bcl-2-associated X protein (BAX) expression (p < 0.05). Furthermore, LN19184 significantly upregulated brain-derived neurotrophic factor (BDNF), phosphorylated cAMP response element-binding protein (p-CREB), and a disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) expression (p < 0.05), suggesting enhanced neuroprotection and synaptic plasticity.
CONCLUSION: LN19184 mitigated LPS-induced neuroinflammation, oxidative stress, apoptosis-related signaling, and neuronal dysfunction markers, while improving cognitive performance in rats. These findings suggest that LN19184 exerts neuroprotective effects and warrants further investigation for its potential to mitigate inflammation-associated neuronal dysfunction.
METHODS: The antioxidant and acetylcholinesterase (AChE) inhibitory activities of LN19184 were assessed and compared with those of the individual plant extracts. Acetylcholine (ACh) levels were measured in SH-SY5Y neuronal cells. In LPS-stimulated cells, the effects of LN19184 on nuclear factor kappa B (NF-κB) phosphorylation, Tau phosphorylation, and β-secretase 1 (BACE-1) expression were evaluated. In vivo, Sprague Dawley rats were challenged with LPS and treated with LN19184. Behavioral assessments of spatial learning, working memory, and recognition memory were conducted. Hippocampal oxidative stress, inflammatory markers, apoptosis-related proteins, and neurodegenerative or synaptic plasticity-associated proteins were analyzed.
RESULTS: LN19184 exhibited greater (p < 0.05) superoxide anion scavenging and AChE inhibitory activities than the individual extracts and increased ACh levels in SH-SY5Y cells. In LPS-stimulated cells, LN19184 significantly reduced NF-κB phosphorylation, Tau phosphorylation, and BACE-1 expression (p < 0.05). In LPS-challenged rats, LN19184 significantly improved spatial learning, working memory, and recognition memory compared with the LPS control group (p < 0.05). These behavioral benefits were accompanied by reduced hippocampal oxidative stress and lower levels of inflammatory markers. LN19184 supplementation increased hippocampal B-cell lymphoma 2 (Bcl-2) and reduced caspase-3 and Bcl-2-associated X protein (BAX) expression (p < 0.05). Furthermore, LN19184 significantly upregulated brain-derived neurotrophic factor (BDNF), phosphorylated cAMP response element-binding protein (p-CREB), and a disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) expression (p < 0.05), suggesting enhanced neuroprotection and synaptic plasticity.
CONCLUSION: LN19184 mitigated LPS-induced neuroinflammation, oxidative stress, apoptosis-related signaling, and neuronal dysfunction markers, while improving cognitive performance in rats. These findings suggest that LN19184 exerts neuroprotective effects and warrants further investigation for its potential to mitigate inflammation-associated neuronal dysfunction.