BackgroundPresent study evaluates the neuroprotective effect of β-elemene alone and in combination with hyperbaric oxygen (HO) in traumatic brain injury (TBI).MethodologyTBI was induced by dropping a weight from a specific height. All the animals were separated in to five groups (n=20) like control group; TBI group; β-elemene treated group which receives β-elemene (100 mg/kg, i.p.) half an hour after the injury; HO group which receives hyperbaric oxygen therapy and β-elemene + HO group which receives β-elemene (100 mg/kg, i.p.) half an hour after the injury and hyperbaric oxygen therapy. Neurological function was assessed to evaluate the effect of β-elemene in TBI rats. Thereafter level of inflammatory cytokines and expression of protein of inflammatory pathway was assessed in the brain tissues of TBI rats. In addition TUNEL assay was also done for the determination apoptosis in neuronal cells.ResultData of the report reveals that β-elemene alone and in combination with hyperbaric oxygen (HO) significantly decreases the neurological score Compared to TBI group. Moreover level of inflammatory cytokines and expression of LTR4 and casepase 3 significantly decrease and increase in the expression of IkB in β-elemene alone and in combination with hyperbaric oxygen (HO) treated group compared to TBI group. Data of TUNEL assay also reveals that β-elemene treated group shows significant decrease in the TUNEL positive cells and apoptosis index compared to TBI group.ConclusionThus present study concludes the neuroprotective effect of β-elemene against TBI and it shows synergistic effect on TBI when treated with HO.

Diabetic peripheral neuropathy (DPN) is a complex disorder caused by long-standing diabetes. Oxidative stress was considered the critical creed in this DPN pathophysiology. Hydrogen has antioxidative effects on diabetes mellitus and related complications. However, there is still no concern on the beneficial effects of hydrogen in DPN. This paper aimed to evaluate the effects of exogenous hydrogen to reduce the severity of DPN in streptozotocin-induced diabetic rats. Compared with hydrogen-rich saline treatment, hydrogen inhalation significantly reduced blood glucose levels in diabetic rats in the 4 th and 8 th weeks. With regard to nerve function, hydrogen administration significantly attenuated the decrease in the velocity of motor nerve conduction in diabetic animals. In addition, hydrogen significantly attenuated oxidative stress by reducing the level of malondialdehyde, reactive oxygen species, and 8-hydroxy-2-deoxyguanosine and meaningfully enhanced the antioxidant capability by partially restoring the activities of superoxide dismutase. Further studies showed that hydrogen significantly upregulated the expression of nuclear factor erythroid-2-related factor 2 and downstream proteins such as catalase and hemeoxygenase-1 in the nerves of diabetic animals. Our paper showed that hydrogen exerts significant protective effects in DPN by downregulating oxidative stress via the pathway of nuclear factor erythroid-2-related factor 2, which suggests its potential value in clinical applications.

Purpose: To investigate the effect of bisleuconothine A (BA), alone and in combination with hyperbaric oxygen (HO), on traumatic brain injury (TBI) in rats. Methods: Traumatic brain injury (TBI) was induced by dropping a 200-g weight of steel on the left anterior frontal areas of Sprague-Dawley rats. The synergistic effect of BA and HO was determined by assessing neurological score, as well as parameters of oxidative stress and inflammation, expressions of P2X4 protein and other proteins, and levels of reactive oxygen species (ROS) in the brain tissues of TBI rats. Results: Neurological function score, levels of inflammatory mediators and oxidative stress parameters were significantly reduced in rats treated with BA alone, and in those treated with a combination of BA and HO, when compared with untreated TBI rats (p < 0.01). Moreover, treatment with BA alone, and BA-HO combination attenuated the altered protein expressions of P2X4, Akt, PI3K and TLR-4 in the TBI rats, and also upregulated the mRNA expression of P2X4 in the brain tissue, when compared with untreated TBI rats (p < 0.01). Conclusion: These results suggest that BA, when used alone or in combination with HO, reduces neuronal injury through upregulation of the protein expression of P2X4 in rats with traumatic brain injury. Thus, BA may be used clinically with HO therapy for the management of traumatic injury. Keywords: Bisleuconothine A, Hyperbaric oxygen, Neuronal injury, Oxidative stress, Inflammatory mediators

Purpose: To study the efficacy of glucocorticoid combined with hyperbaric oxygen therapy for the treatment of delayed encephalopathy after carbon monoxide poisoning (DEACMP), and its effect on the expression of immune-associated cytokines. Methods: A total of 102 DEACMP patients in PLA General Hospital, Haidian, China were divided into two groups of 51 patients each, namely, observation group (glucocorticoid + hyperbaric oxygen therapy), and control group (hyperbaric oxygen only). The clinical data for each group was retrospectively analyzed. Clinical efficacy, improvement time, hospitalization time, cognitive function, activities associated with daily living, changes in immunity-associated cytokines, and incidence of adverse reactions were compared for the two groups. Results: Following treatment, the time taken for improvement, duration of hospitalization, cognitive function, daily living activity and total effectiveness in the observation group were significantly higher than those for the control group (p < 0.05). In addition, the levels of transforming growth factor beta 1 (TGF-β1), interleukin 4 (IL-4) and interferon-gamma (IFN-γ) in the observation group were significantly greater than for the corresponding control group levels (p <0.05). There was no significant difference in incidence of adverse reactions between the two groups (p > 0.05). Conclusion: These results suggest that a combination therapy of glucocorticoid and hyperbaric oxygen therapy for the treatment of DEACMP is more eutherapeutic in the improvement of cognitive function and activities of daily living in DEACMP patients than hyperbaric oxygen therapy. The mechanism of this combination therapy may be related to the improvement in immunity-related cytokine levels.

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