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Traumatic brain injury (TBI) is one of the most causes of death and disability among people, leading to a wide range of neurological deficits. The important process of neurogenesis in the hippocampus, which includes the production, maturation and integration of new neurons, is affected by TBI due to microglia activation and the inflammatory response. During brain development, microglia are involved in forming or removing synapses, regulating the number of neurons, and repairing damage. However, in response to injury, activated microglia release a variety of pro-inflammatory cytokines, chemokines and other neurotoxic mediators that exacerbate post-TBI injury.These microglia-related changes can negatively affect hippocampal neurogenesis and disrupt learning and memory processes. To date, the intracellular signaling pathways that trigger microglia activation following TBI, as well as the effects of microglia on hippocampal neurogenesis, are poorly understood. In this review article, we discuss the effects of microglia-induced neuroinflammation on hippocampal neurogenesis following TBI, as well as the intracellular signaling pathways of microglia activation.

IntroductionAnethole is the main compound of the essential oil of anise and several other plants, which has antioxidant, anti-inflammatory, and neuroprotective properties. Oxidative stress is considered as an important factor in the pathogenesis of PD. In the present study, we aimed to investigate the effects of anethole against rotenone-induced PD.MethodsMale Wistar rats were randomly divided into six groups. Control group received DMSO + sunflower oil, model group received rotenone (2 mg/kg, s.c, daily for 35 days), positive control group received L-Dopa, and test groups received anethole (62.5, 125, and 250 mg/kg, i.g, daily for 35 days) 1 hour before each rotenone injection. Body weight changes, rotarod test, stride length test, and extracellular single unit recording were performed after treatment. After behavioral test, Brain water content and blood brain barrier (BBB) permeability were evaluated, and the levels of malondialdehyde (MDA), superoxide dismutases (SOD), alpha-synuclein and MAO-B were measured in the striatum.ResultsChronic administration of rotenone induced body weight loss and caused significant dysfunction in locomotor activity, neuronl firing rate, and BBB. Rotenone also decreased SOD activity, increased MDA level, and elevated the expression of alpha-synuclein and MAO-B in the striatum. However, treatment with anethole attenuated body weight loss, motor function, neuronal activity, and BBB function. Furthermore, Anethole treatment attenuated oxidative stress and decreased the expression of alpha-synuclein and MAO-B compared to the rotenone group.ConclusionOur results show that through its antioxidant properties, aethole can improve the cellular, molecular and behavioral characteristics of rotenone-induced Parkinson's disease.