Background
People who experience traumatic events have an increased risk of post-traumatic stress disorder (PTSD). However, PTSD-related pathological changes in the hippocampus and prefrontal cortex remain poorly understood.

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Glutamate and GABA imbalance promotes neuronal apoptosis in hippocampus after stress

Purpose Brain stroke is a leading cause of death without effective treatment. B. monniera, an Indian herbal medicine, exerts antioxidant activity and antistress activity by modulating the antioxidative defence system. We wanted to test if B. monniera could alleviate the ischemia induced brain injury and cognitive dysfunction in Wistar rats. Procedure We studied the effect of B. monniera (120 mg kg− 1, 160 mg kg− 1 and 240 mg kg− 1 P.O.) on transient intracarotid artery (ICA) occlusion induced ischemia by testing the neurobehavioral and biochemical parameters on treated and control rats. Findings B. monniera attenuated the reduced transfer latency in ischemic rats in a step through test and showed a protective effect on ischemia induced memory impairment in the plus maze task. It also showed a marginal improvement in neurodeficit score and fore limb muscle grip strength. B. monniera reduced the infarct size in the ischemic brain. It also decreased nitrite, nitrate and lipid peroxidation and significantly improved catalase activity. Conclusion These observations suggest the neuroprotective and antioxidant activity of B. monniera on ischemia induced brain injury and pave the way for future investigations.

Neuroprotective effect of Bacopa monniera on ischemia induced brain injury

Due to numerous industrial applications, lead has caused widespread pollution in the environment; it seems that the central nervous system (CNS) is the main target for lead in the human body. Oxidative stress and programmed cell death in the CNS have been assumed as two mechanisms related to neurotoxicity of lead. Cerium oxide (CeO2) and yttrium oxide (Y2O3) nanoparticles have recently shown antioxidant effects, particularly when used together, through scavenging the amount of reactive oxygen species (ROS) required for cell apoptosis. We looked into the neuroprotective effects of the combinations of these nanoparticles against acute lead-induced neurotoxicity in rat hippocampus. We used five groups in this study: control, lead, CeO2 nanoparticles + lead, Y2O3 nanoparticles + lead, and CeO2 and Y2O3 nanoparticles + lead. Nanoparticles of CeO2 (1000 mg/kg) and Y2O3 (230 mg/kg) were administered intraperitoneally during 2 days prior to intraperitoneal injection of the lead (25 mg/kg for 3 days). At the end of the treatments, oxidative stress markers, antioxidant enzymes activity, and apoptosis indexes were investigated. The results demonstrated that pretreatments with CeO2 and/or Y2O3 nanoparticles recovered lead-caused oxidative stress markers (ROS, lipid peroxidation, and total thiol molecules) and apoptosis indexes (Bax/Bcl-2 and caspase-3 protein expression). Besides, these nanoparticles reduced the activities of lead-induced superoxide dismutase and catalase as well as the ADP/ATP ratio. Interestingly, the best recovery resulted from the compound of these nanoparticles. Based on these outcomes, it appears that this combination may potentially be beneficial for protection against lead-caused acute toxicity in the brain through improving the oxidative stress-mediated programmed cell death pathway.

Cerium and Yttrium Oxide Nanoparticles Against Lead-Induced Oxidative Stress and Apoptosis in Rat Hippocampus

Perinatal exposure to lead induces morphological, ultrastructural and molecular alterations in the hippocampus.

Ascorbic acid ameliorates oxidative damage induced by maternal low-level lead exposure in the hippocampus of rat pups during gestation and lactation.

Protective effects of ascorbic acid against lead-induced apoptotic neurodegeneration in the developing rat hippocampus in vivo.

This research investigated whether exposure of diesel exhaust particulate (DEP) and particulate matter (PM) effects on airway remodeling in asthma induced Balb/c and IL-10 knock out (KO) mouse. Mice were sensitized with intraperitoneal injection with ovalbumin, followed by challenges with intranasal ovalbumin. After that mice placed in inhalation chamber and exposed to DEP and . The evidence of airway remodeling was assessed by masson`s trichrome staining and PAS staining. The stainability of masson`s trichrome and PAS reaction were increased in asthma-induced Baltic mice groups compared with control mice groups. More intensive stainability for masson`s trichrome and PAS were appeared in the asthma-induced DEP and PM-exposed groups than asthama-induced groups. But, not significantly increased subepithelial fibrosis and the nember of goblet cell hyperplasia in asthma-induced IL-10 KO mice groups and asthma-induced+DEP and PM-exposed IL-10 KO mice than IL-10 KO mice groups. These results indirectly suggesting that exposure to DEP and PM in asthmatic patients might be aggravate clinical symptoms and IL-10 which seems to play a central role in allergic asthma. In conclusion, DEP and PM exposure might have additive effects on the ovalbumin- induced asthma in a murine model.

Tian-Zhu Li

Papers

Protective effects of ascorbic acid against lead-induced apoptotic neurodegeneration in the developing rat hippocampus in vivo.

The Effects of Diesel Exhaust Particulates and Particulate Matters on the Airway Remodeling in the Asthma-induced Mice