Recently, studies conducted with astrocyte cells have drawn attention to neurodegeneration pathologies caused by aluminum exposure. In particular, investigating the potential of herbal therapeutic agents to prevent this effect of aluminum has gained importance. The purpose of this study was to investigate the therapeutic and preventive effects of piperine, curcumin, and the combination of these compounds on reactive primary astrocyte cells. In order to examine the preventive effect, certain concentrations of compounds were applied to the cells before the aluminum application, and to be able to determine the therapeutic effect, the compounds were examined after the aluminum application. The efficacy of the compounds was analyzed in terms of cell viability, apoptosis, necrosis, and cytokine release. In conclusion, the results of the study showed that the use of different concentrations of piperine, curcumin, and their combination had significantly higher % cell viability on aluminum-induced damage in astrocyte cells compared to the damaged control group. In addition, a decrease in the number of apoptotic and necrotic cells was observed in the same groups, which indicated that piperine increased curcumin activity. The decrease in the amount of IL-6 and TGF-β cytokines also supported that piperine increased the effectiveness of curcumin. Considering all these results, it can be said that in terms of aluminum damage in astrocyte cells, the bioavailability-enhancing property of piperine on curcumin was shown for the first time in the literature. In line with these results, it is inevitable to carry out further studies.
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http://dx.doi.org/10.1007/s12640-022-00600-9 | DOI Listing |
Bull Exp Biol Med
January 2025
Research Center of Neurology, Moscow, Russia.
The number of microglia cells and astrocytes in layer V of the cerebral cortex was estimated on day 7 after damage caused by a unilateral focal traumatic brain injury of the left hemisphere sensorimotor cortex. Quantitative assessment was performed by counting immunocytochemically stained microglia cells (Iba1 marker) and activated astrocytes (GFAP) at different distances from the lesion site. Activation of microglial and astroglial cells was observed not only in the marginal zone of the lesion of the left hemisphere, but also in the intact hemisphere.
View Article and Find Full Text PDFNat Neurosci
January 2025
Centre for Discovery Brain Sciences, University of Edinburgh, Edinburgh, UK.
Brain-resident macrophages, microglia, have been proposed to have an active role in synaptic refinement and maturation, influencing plasticity and circuit-level connectivity. Here we show that several neurodevelopmental processes previously attributed to microglia can proceed without them. Using a genetically modified mouse that lacks microglia (Csf1r), we find that intrinsic properties, synapse number and synaptic maturation are largely normal in the hippocampal CA1 region and somatosensory cortex at stages where microglia have been implicated.
View Article and Find Full Text PDFCell Mol Life Sci
January 2025
Shanghai Key Laboratory of Anesthesiology and Brain Functional Modulation, Clinical Research Center for Anesthesiology and Perioperative Medicine, Translational Research Institute of Brain and Brain-Like Intelligence, Department of Anesthesiology and Perioperative MedicineSchool of Medicine, Shanghai Fourth People's Hospital, School of Medicine, Tongji University, 1239 Sanmen Road, Hongkou District, Shanghai, 200434, China.
Background: Perioperative neurocognitive disorder (PND) is a prevalent form of cognitive impairment in elderly patients following anesthesia and surgery. The underlying mechanisms of PND are closely related to perineuronal nets (PNNs). PNNs, which are complexes of extracellular matrix primarily surrounding neurons in the hippocampus, play a critical role in neurocognitive function.
View Article and Find Full Text PDFChin J Integr Med
January 2025
Department of Anaesthesiology, Nanjing Drum Tower Hospital, Nanjing Drum Tower Hospital Clinical College, Nanjing University of Chinese Medicine, Nanjing, 210008, China.
Objective: To illustrate the role of dehydrocorydaline (DHC) in chronic constriction injury (CCI)-induced neuropathic pain and the underlying mechanism.
Methods: C57BL/6J mice were randomly divided into 3 groups by using a random number table, including sham group (sham operation), CCI group [intrathecal injection of 10% dimethyl sulfoxide (DMSO)], and CCI+DHC group (intrathecal injection of DHC), 8 mice in each group. A CCI mouse model was conducted to induce neuropathic pain through ligating the right common sciatic nerve.
Sci Rep
January 2025
Children's Research Center, Division of Oncology, University Children's Hospital Zürich, Zürich, Switzerland.
De-regulated protein expression contributes to tumor growth and progression in medulloblastoma (MB), the most common malignant brain tumor in children. MB is associated with impaired differentiation of specific neural progenitors, suggesting that the deregulation of proteins involved in neural physiology could contribute to the transformed phenotype in MB. Calsynthenin 1 (CLSTN1) is a neuronal protein involved in cell-cell interaction, vesicle trafficking, and synaptic signaling.
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