Triptolide mediates Wnt/ß-catenin signalling pathway to reduce cerebral ischemia-reperfusion injury in rats.

INTRODUCTION: Triptolide, extracted from Chinese medicinal materials Tripterygium wilfordii Hook F (TwHF), has immunosuppressive, anti-inflammatory and anti-tumour effects. The purpose of this study was to examine whether triptolide has the neuroprotective effect on cerebral ischemia-reperfusion (I/R) injury and to explore its possible mechanism. MATERIAL AND METHODS: The rat model of focal cerebral I/R was established by the suture-occluded method. The SD rats were randomly divided into five groups: sham operation group (Sham group), ischemia-reperfusion model group (I/R group), low concentration of triptolide group (12.5 mg/kg, TL-L group), medium concentration of triptolide group (25 mg/kg, TL-M group) and high concentration of triptolide group (50 mg/kg, TL-H group). The neurological function of the rats was scored, the degree of brain oedema was detected by the dry-wet method, and the cerebral infarction area was determined by TTC staining. Nissl staining was used to detect neuronal damage. The contents of reactive oxygen species (ROS), malondialdehyde (MDA) and superoxide dismutase (SOD) were also detected. Meanwhile, the expression level of proteins related to Wnt/-catenin signalling pathway was measured by Western blot. RESULTS: Compared with the I/R group, cerebral oedema, infarct volume, neurological impairment, the contents of MDA and ROS were reduced, while the SOD level was increased in the TL-L, TL-M, and TL-H groups. The results of Nissl staining showed that triptolide could reduce the nerve cell injury caused by cerebral I/R. In addition, the results of Western blot confirmed that the expression of Wnt1, -catenin, c-Myc, and Cyclin-D1 were down-regulated after triptolide intervention, that is, inhibited the activation of Wnt/-catenin signalling pathway. CONCLUSIONS: Triptolide mediates Wnt/-catenin signalling pathway to alleviate cerebral I/R injury in rats. This study provides ideas and experimental basis for the treatment of ischemic stroke patients.

Protective Effect of Diphenhydramine against Traumatic Brain Injury in Rats via Modulation of Oxidative Stress and Inflammation.

BACKGROUND: Traumatic brain injury (TBI) is considered a major burden across the globe affecting both individuals and their families. Therefore, the present study was conducted to determine the protective effect of diphenhydramine (DPM) against TBI in experimental rats. METHODS: The effect of DPM was evaluated on the cerebral edema (CE) and neuronal degeneration after the induction of experimental brain injury in rats. The effect of DPM was also investigated on the inflammatory cytokines, for example, tumor necrosis factor-α and interleukin 1ß and oxidative stress markers, such as malondialdehyde, superoxide dismutase, and glutathione peroxidase. Western blot analysis was used to investigate the effect of DPM on B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax) and cleaved caspase-3. RESULTS: Results of the study suggest that DPM causes reduction in CE and prevents neuronal degeneration. It also causes reduction in inflammation and oxidative stress in a dose-dependent manner. The level of Bax was found to be elevated, together with reduction in the Bcl-2 level in the DPM-treated group. CONCLUSION: DPM exerts a neuroprotective effect after TBI via the attenuation of oxidative stress, inflammation, and mitochondrial apoptosis pathways.

Efficacies of minimally invasive puncture and small bone window craniotomy for hypertensive intracerebral hemorrhage, evaluation of motor-evoked potentials and comparison of postoperative rehemorrhage between the two methods.

Application value of the minimally invasive puncture and small bone window craniotomy in hypertensive intracerebral hemorrhage was investigated to explore the effects of the above treatment methods on motor-evoked potentials (MEPs) and postoperative rehemorrhage. Patients with hypertensive intracerebral hemorrhage who were admitted to Chengyang People's Hospital from March 2016 to December 2017 were selected and randomly divided into the minimally invasive group (n=40) and the craniotomy group (n=40). The minimally invasive group was treated with minimally invasive puncture and drainage for hematomas, while the craniotomy group received small bone window craniotomy for evacuation of hematomas. The clinical efficacy was compared between the two groups. At 28 days after operation, the Chinese scale of clinical neurological deficit of stroke patients (CSS) score in the minimally invasive group was lower than that in the craniotomy group (p<0.05). At 28 days after operation, the S-100ß level in the minimally invasive group was lower than that in the craniotomy group (p<0.05). At 1 week after operation, 35 patients in the minimally invasive group were able to elicit MEP waveforms, and only 7 patients in the craniotomy group were able to elicit positive waveforms. At 2 weeks after operation, 40 patients in the minimally invasive group and 20 patients in the craniotomy group could elicit MEP waveforms, and the incubation period, central motor conduction time and amplitude in the former were significantly better than those in the latter (p<0.05). The operation time and length of hospital stay were shorter with more total expenses of hospitalization in the minimally invasive group compared to those in the craniotomy group (p<0.05). Compared with small bone window craniotomy, minimally invasive puncture can reduce serum S-100ß level. Its advantages are obvious, so it is worthy of promotion and application.