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Microplastic particles in the blood can cause damage to organs such as the brain. This study aimed to analyze the effect of microplastic particles in the blood on membrane damage (expression of malondialdehyde metabolites) and deoxyribonucleic acid damage (expression of 8-hydroxy-2′-deoxyguanosine metabolites) in hippocampus neurons of Wistar rats. Methods: Forty-two Wistar rats were used and equally divided into six groups. The study groups X1, X2, X3, X4 and X5 was given 0.0375mg, 0.075mg, 0.15mg, 0.3mg, and 0.6mg of low-density polyethylene microplastic powder mixed with 2cc distilled water respectively, while the control group only given distilled water. Microplastic administration was carried out for 90 days. Results: Microplastic particles were found in the blood of Wistar rats. The level of microplastics particle was higher along with the higher exposure dose. The mean expression of malondialdehyde and 8-hydroxy-2′-deoxyguanosine metabolites in the hippocampal neurons in CA1 and CA3 areas were significantly increased with higher exposure doses (Kruskal-Wallis test p <0.01). The Spearmen’s correlation showed a strong relationship between the levels of microplastic particles in blood and the expression of metabolites malondialdehyde and 8-hydroxy-2′-deoxyguanosine (all p <0.01). Microplastic in the blood of Wistar rats has increased expression of malondialdehyde and 8-hydroxy-2′-deoxyguanosine metabolites in hippocampal neurons.

Background Spinal cord injury (SCI) is a significant cause of morbidity since it results in the inflammation process which leads to necrosis or apoptosis. Inflammatory response to the tissue damage increases IL-6 and IL-8 levels. ACTH4–10Pro8-Gly9-Pro10 is a peptide community that has been shown to have a beneficial effect on minimizing the morbidity and increasing the recovery time. Methods This study is a true experimental laboratory research with a totally randomized method. The subjects were animal models with light and extreme compression of spinal cord, respectively. Results The administration of ACTH 4–10 in mild SCI in the 3-hour observation group did not show a significant difference in IL-6 expression compared with the 6-hour observation group. The administration of ACTH 4–10 in severe SCI showed a significantly lower expression level of IL-6 in the 3-hour observation group compared with the 6-hour one. The administration of ACTH 4–10 in severe SCI led to a significantly lower IL-8 expression in the 3-hour observation group compared with the 6-hour one. However, there was no significant difference in IL-8 expression in the group receiving ACTH 4–10 in 3 hours observation compared with that in 6 hours observation. Conclusion The administration of ACTH4–10Pro8-Gly9-Pro10 can reduce the expression of IL-6 and IL-8 at 3-hour and 6-hour observation after mild and severe SCI in animal models. Future research works are recommended.

Background: Globally, spinal cord injury (SCI) results in a big burden, including 90% suffering permanent disability, and 60%-69% experiencing neuropathic pain. The main causes are oxidative stress, inflammation, and degeneration. The efficacy of the stem cell secretome is promising, but the role of human neural stem cell (HNSC)secretome in neuropathic pain is unclear. This study evaluated how the mechanism of HNSC-secretome improves neuropathic pain and locomotor function in SCI rat models through antioxidant, anti-inflammatory, anti-matrix degradation, and neurotrophic activities. Methods: A proper experimental study investigated 15 Rattus norvegicus divided into normal, control, and treatment groups (30 µL HNSC-secretome, intrathecal in the level of T10, three days post-traumatic SCI). Twentyeight days post-injury, specimens were collected, and matrix metalloproteinase (MMP)-9, F2-Isoprostanes, tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β, and brain derived neurotrophic factor (BDNF) were analyzed. Locomotor recovery was evaluated via Basso, Beattie, and Bresnahan scores. Neuropathic pain was evaluated using the Rat Grimace Scale. Results: The HNSC-secretome could improve locomotor recovery and neuropathic pain, decrease F2-Isoprostane (antioxidant), decrease MMP-9 and TNF-α (anti-inflammatory), as well as modulate TGF-β and BDNF (neurotrophic factor). Moreover, HNSC-secretomes maintain the extracellular matrix of SCI by reducing the matrix degradation effect of MMP-9 and increasing the collagen formation effect of TGF-β as a resistor of glial scar formation. Conclusions: The present study demonstrated the mechanism of HNSC-secretome in improving neuropathic pain and locomotor function in SCI through antioxidant, anti-inflammatory, anti-matrix degradation, and neurotrophic activities.

Background: The purpose of this study was to analyze the response of inflammatory cytokines interleukin-8 (IL-8) and NF-κB to the closure of skull defect with periosteum as a scaffolding material in bone healing used after surgery. Methods: Thirty Oryctolagus cuniculus rabbits underwent a craniotomy to create a 20 mm diameter round defect in the parietal bones. The parietal bones were returned to its place and stabilized by an internal plate fixation. The defects were either left empty or implanted with periosteum. At 6 weeks, the specimens were euthanized and examined. Results: Histological examination showed a more well-developed formation of woven bone in the periosteum group. Immunohistochemical examinations showed that the use of periosteum in the closure of skull defects reduced the NF-κB and IL-8 response which affected the ossification process. Conclusion: The experiment showed that the use of periosteum was linked with IL-8 and NF-κB downregulation toward ossification effects at any point throughout the trial. Periosteum usage might be beneficial as a scaffolding material in bone healing for autograft cranioplasty in animal model and could be applied to clinical practice.

This study aims to investigate the effects of treatment with human neural stem cell (HNSC) secretomes on subacute spinal cord injury (SCI) post-laminectomy by analyzing interleukin-10 (IL-10), matrix metalloproteinase 9 (MMP9), transforming growth factor-β (TGF-β), and Basso-Beattie-Bresnahan (BBB) score locomotors as expressions of neurological recovery. Overview of Literature: In the United States, SCI has a recovery rate of 0.08%, tetraplegia 58.7%, and paraplegia 40.6%. Therapeutic approaches to SCI have focused on modulating the secondary cascade to prevent neurological deterioration and glial scar formation. Increasing evidence has shown that the success of cell-based SCI therapy is attributed to the secretomes rather than the cells themselves, but the effect of treatment with HNSC secretomes in SCI is unclear. Methods: This experimental study investigated 15 Rattus norvegicus rats that were divided into three groups: (1) normal, (2) SCI+nonsecretome, and (3) SCI+secretome (30 µL, intrathecal Th10). Model subacute SCI post-laminectomy was performed in 60 seconds using an aneurysm Yasargil clip with a closing forceps weighing 65 g (150 kdyn). At 35 days post-injury, the specimens were collected, and the immunohistochemicals of IL-10, MMP9, and TGF-β were analyzed. Motor recovery was evaluated based on the BBB scores. Results:The SCI post-laminectomy of rats treated with HNSC secretomes showed improvements in their locomotor recovery based on the BBB scores (p=0.000, mean=18.4) and decreased MMP9 (p=0.015) but had increased the levels of IL-10 (p=0.045) and TGF-β (p=0.01). Conclusions: These results indicate that the factors associated with the HNSC secretomes can mitigate their pathophysiological processes of secondary damage after SCI and improve the locomotor functional outcomes in rats.

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Low-density polyethylene microplastics are ingested into the bloodstream and distributed to all the organ tissue, including the hippocampus, causing toxic effects. This research aimed to elucidate the responses of hippocampal neurons to microplastic in the blood based on the expressions of superoxide dismutase (SOD), catalase (CAT) enzymes, malondialdehyde (MDA), 8-oxo-7,8-dihydro-2-deoxyguanosine (8-OHdG) in hippocampal neurons, and blood serum amyloid beta 1-42 (Aβ42) levels using SMART PLS pathway analysis. Methods: This was a pure experimental research on Wistar rats with a post-test control group design. Five experimental groups (X1, X2, X3, X4, X5) were given 0.0375 mg, 0.075 mg, 0.15 mg, 0.3 mg, and 0.6 mg of low-density polyethylene microplastics mixed in 2cc distilled water, respectively. Furthermore, except for control (C), the groups received microplastics an oral probe for 90 days. Results: The molecular response of hippocampal neurons of Wistar rats to microplastics in the blood significantly decreased SOD enzyme expression, while CAT enzyme was unaffected. It considerably increased neuronal membrane damage (expression of MDA), increased considerably neuronal deoxyribonucleic acid damage (expression of 8-OHdG), and decreased blood serum Aβ42 levels (pathway analysis, all t-value >1.96). Conclusion:The pathway analysis showed that hippocampal neurons were significantly affected by microplastic particles in the blood.