@article {1494, title = {Evaluation of Neuroprotective Potential of Water-Dispersible Turmeric Extract and Sustained-Release Ashwagandha Root Extract against B[A]P Induced Neurotoxicity in Zebrafish}, journal = {Pharmacognosy Research}, volume = {17}, year = {2025}, month = {August 2025}, pages = {1218-1225}, type = {Original Article}, chapter = {1218}, abstract = {

Background: Numerous advantages of using herbs in the management of neurodegenerative disorders have been documented. Water-Dispersible Turmeric Extract Containing 60\% Natural Curcuminoids (WDTE60N) and Sustained-Release Ashwagandha Root Extract (AshwaSR) are the herbal formulations prepared from the extracts of turmeric rhizome and Ashwagandha root, respectively. Benzo[a]pyrene (B[a]P), a polycyclic aromatic hydrocarbon, has recently emerged as a neurotoxic compound that impacts zebrafish behaviour and triggers oxidative stress. This neurotoxic effect illustrates the link between oxidative stress and neurodegeneration, as well as the development of anxiety-like behaviours in zebrafish. This study aimed to investigate the neuroprotective potential of WDTE60N and AshwaSR against B[a]P-induced neurotoxicity in zebrafish. Materials and Methods: In geometric sequence, 5 different concentrations of each formulation were prepared and administered to zebrafish for 7 days via bath immersion technique. Before the administration of active concentration, fish were exposed to B[a]P for seven days. Neurobehavioral patterns were assessed by using novel tank diving test and light and dark box test. Results: Exposure to B[a]P for seven days reduced the locomotor activity of zebrafish and increased their preference for the lighter part of the glass tank. A notable increase in locomotor activity and higher preference for diving towards lower zone of tank was observed in the zebrafish treated with WDTE60N or AshwaSR. The histopathological findings showed that supplementation with these herbal formulations resulted in reduction in congestion of the corpus cerebella region of adult zebrafish brain. Conclusion: Collectively, WDTE60N and AshwaSR demonstrated neuroprotective potential against B[a]P-induced neurobehavioral alterations in the zebrafish.

}, keywords = {Ashwagandha, B[a]P, Neurobehavioral, Neurodegeneration, Turmeric, Zebrafish}, doi = {10.5530/pres.20252280}, author = {Tushar Lokhande and Madhusudan Saraf and Jaya Agnihotri and Nikhat Khan and Tejal Dhotre and Sneha Sawant Desai and Ritik Singh} } @article {1134, title = {Possible Involvement of Cellular Pathway and Cytokines in Manganese Induced Neurotoxicity in Neuroblastoma Cells via KH{\textendash}Type Splicing Regulatory Protein}, journal = {Pharmacognosy Research}, volume = {15}, year = {2023}, month = {February 2023}, pages = {307-314}, type = {Original Article }, chapter = {307}, abstract = {

Background: Manganese is a toxic essential trace element and too high concentration instigates the neurodegenerative disease known as parkinsonism. Effects of manganese may lead to apoptosis. However, a detailed mechanism of manganese toxicity has not been fully elucidated. Previous published articles have highlighted the augmentation of KHSRP expression following Mn exposure. Objectives: In this work, the importance of KHSRP in Mn{\textendash}induced toxicity was checked along with the impact of other known neurotoxicity inhibitors on KHSRP. Materials and Methods: KHSRP expression, pro and anti-inflammatory cytokines, chemokines, and pharmacological inhibitors (SAHA, Quercetin, and MCC950) were determined by exposing N2a cells to various MnCl2 concentrations. ANOVA and Dunnett{\textquoteright}s test were used to decide on the significance. Results: MnCl2 treatment led to the augmentation of the KHSPR mRNA expression and protein increase in N2a cell line. The MnCl2 treatment of N2a cells also showed an elevated liberation of IL-6, TNF-α, MCP{\textendash}1, and IL-1β. Pharmacological agents like quercetin inhibiting PI3K, MAPK, and WNT pathways, MCC950 blocking NLRP3 pathways, and SAHA showed a decrease in KHSRP expression post Mn treatment. With the inhibition of KHSRP, a decline in the release of IL-1β, IL-6, MCP{\textendash}1, and TNF-α was also observed. Conclusion: These results suggested that MnCl2 treatment of N2a cells induce the expression of KHSRP via the PI3K{\textendash}or NLRP3 pathway. Furthermore, this elevated expression of KHSRP is responsible for an increment in the liberation of pro-inflammatory markers in N2a cells. More exploration is needed to throw light on the pathway driving the KHSRP.

}, keywords = {KH{\textendash}type Splicing Regulatory Protein, Manganese Neurotoxicity, Neuroblastoma, Neurodegeneration, Neuroinflammation.}, doi = {10.5530/pres.15.2.033}, author = {Sharad Singh and Sunil More and G. S. Latha and Himanshu Agrawal and Veena S M and Francois Niyonzima} }