Journal of Clinical and Basic Research (Jul 2023)
Hippocampal overexpression of IL-1β and TNF-α associated with Zinc loss secondary to psychological stress is mitigated in probiotic-treated rats
Abstract
Background: Psychological stress (PS) disrupts the gut microbiome, accelerates cognitive decline, and causes a predisposition to certain neurodegenerative diseases. This study was designed to test the hypothesis that the administration of probiotics has beneficial effects on the neurohistology and neurochemistry of the hippocampus following exposure to psychological stress (PS). Methods: Thirty-five adult male Wistar rats weighing 180±5g were randomly assigned to seven groups (n=5) comprising the control, acute PS, acute probiotic treatment (probio), acute PS+probio, chronic PS, chronic probio, and chronic PS+probio groups. Acute stress and chronic PS or probio treatment lasted seven and 14 days, respectively. Each animal in the probio groups was fed 10×106 colony-forming units of lactobacillus acidophilus every other day. In contrast, the PS groups were exposed to predator stress for one hour between 7-10 am daily. The treatments lasted for 14 days. Following euthanasia, blood and hippocampal samples were collected for histology, and ELISA-based assays of interleukin-1β (1IL-1β), Tumor Necrosis Factor-α (TNF-α), dopamine, serotonin, malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH). Results: Data analysis reveals that acute and chronic psychological stress significantly depresses hippocampal serotonin and dopamine levels, induces the overexpression of IL-1β and TNF-α, and causes increased lipid peroxidation and impaired antioxidant parameters. The probiotics groups exhibited statistically better results on all parameters assessed, including bringing hippocampal IL-1β and TNF-α levels toward normal. No obvious histoarchitectural damages were observed in any group. Conclusion: Overall, this study suggests that the gut microbiome might play a significant role in hippocampal function as supplementing it mitigates stress-induced perturbations of hippocampal neurochemistry and redox status. Background: Psychological stress (PS) disrupts the gut microbiome, accelerates cognitive decline, and causes a predisposition to certain neurodegenerative diseases. This study was designed to test the hypothesis that the administration of probiotics has beneficial effects on the neurohistology and neurochemistry of the hippocampus following exposure to psychological stress (PS). Methods: Thirty-five adult male Wistar rats weighing 180±5g were randomly assigned to seven groups (n=5) comprising the control, acute PS, acute probiotic treatment (probio), acute PS+probio, chronic PS, chronic probio, and chronic PS+probio groups. Acute stress and chronic PS or probio treatment lasted seven and 14 days, respectively. Each animal in the probio groups was fed 10×106 colony-forming units of lactobacillus acidophilus every other day. In contrast, the PS groups were exposed to predator stress for one hour between 7-10 am daily. The treatments lasted for 14 days. Following euthanasia, blood and hippocampal samples were collected for histology, and ELISA-based assays of interleukin-1β (1IL-1β), Tumor Necrosis Factor-α (TNF-α), dopamine, serotonin, malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH). Results: Data analysis reveals that acute and chronic psychological stress significantly depresses hippocampal serotonin and dopamine levels, induces the overexpression of IL-1β and TNF-α, and causes increased lipid peroxidation and impaired antioxidant parameters. The probiotics groups exhibited statistically better results on all parameters assessed, including bringing hippocampal IL-1β and TNF-α levels toward normal. No obvious histoarchitectural damages were observed in any group. Conclusion: Overall, this study suggests that the gut microbiome might play a significant role in hippocampal function as supplementing it mitigates stress-induced perturbations of hippocampal neurochemistry and redox status.
