The Effects of a Traditional Chinese Medication on Children with Attention-Deficit/Hyperactivity Disorder.

Objective: This feasibility study examined the effects of a particular Traditional Chinese Medicine (TCM) herbal formula on attention-deficit/hyperactivity disorder (ADHD) and related problem behaviors. Design: A total of 79 participants aging 6-12 years consumed a granulated TCM herbal formula twice daily over a period of 3 months and underwent assessments at months 0, 3, and 6. Changes in ADHD symptoms and related behaviors were measured using the ADHD rating scale-IV (ADHD-RS-IV), child behavior checklist (CBCL), children's global sssessment scale (CGAS), as well as the clinical global impressions-severity (CGI-S) and improvement (CGI-I) scales. Results: Repeated measures mixed model analyses revealed significant differences in scores across time on all ADHD-RS-IV and CBCL subscales as well as on the CGAS, CGI-S, and CGI-I scales. Pairwise comparisons between months 0 and 3 as well as months 0 and 6 indicated significant improvements in scores. Scores also did not differ significantly between months 3 and 6. The results may suggest that this particular TCM formula possesses potential therapeutic qualities in the treatment of ADHD. Furthermore, changes in ADHD symptoms generally appear to be stable 3 months after discontinuation. However, these findings could also be attributed to placebo effects as well as reporting biases. Conclusion: This particular TCM formula may prove to be a useful adjunctive treatment for children with ADHD, and randomized controlled trials need to be conducted to evaluate its efficacy.

Proliferation of Bilateral Nerve Fibers Following Thalamic Infarction Contributes to Neurological Function Recovery: A Diffusion Tensor Imaging (DTI) Study.

BACKGROUND The aim of this study was to investigate the reorganization in ipsilesional and contralesional thalamic radiation fibers after unilateral focal thalamic stroke in sensory disturbance patients. MATERIAL AND METHODS We recruited 12 patients with acute unilateral thalamic infarction and sensory disturbance and 12 healthy age- and sex-matched controls. All patients underwent diffusion tensor imaging (DTI) and were assessed with National Institutes of Health stroke scale (NIHSS), Barthel index (BI), and paragraph 8 of NIHSS (NIHSS8) at 1 week (W1), 4 weeks (W4), 3 months (M3), and 6 months (M6) after thalamic infraction. The relationship between FA changes and the clinical scores changes were then examined. RESULTS NIHSS and NIHSS8 scores decreased while BI scores increased gradually from W1 to M6 in patients, but not in controls. FA values of the patients gradually increased in ipsilesional and contralesional thalamic radiation fibers from W1 to M6. In addition, the FA values in patients were significantly higher at M3 and M6 compared to W1. No significant changes were observed in the controls. Regarding the relationship between FA changes and the clinical scores changes, the FA increases were negatively correlated with NIHSS and NIHSS8 decrease while FA increases were positively correlated with BI increases. CONCLUSIONS Our results indicate that reorganization occurred after unilateral focal thalamic infarct not only in ipsilesional, but also in contralesional thalamic radiation fibers in patients with sensory disturbance. In addition, the results suggested that the reorganization can support and promote stroke restoration.

Tongxinluo Enhances Neurogenesis and Angiogenesis in Peri-Infarct Area and Subventricular Zone and Promotes Functional Recovery after Focal Cerebral Ischemic Infarction in Hypertensive Rats.

Background. Tongxinluo is a traditional Chinese medicine compound with the potential to promote the neuronal functional recovery in cerebral ischemic infarction. Objective. This study aimed to disclose whether tongxinluo promotes neurological functional recovery and neurogenesis and angiogenesis in the infarcted area and SVZ after cerebral ischemic infarction in hypertensive rats. Methods. The ischemic model was prepared by distal middle cerebral artery occlusion (MCAO) in hypertensive rats. Tongxinluo was administrated 24 h after MCAO and lasted for 3, 7, or 14 days. Behavioral tests were performed to evaluate the protection of tongxinluo. Immunochemical staining was applied on brain tissue to evaluate the effects of tongxinluo on neurogenesis and vascularization in the MCAO model rats. Results. Postinjury administration of tongxinluo ameliorated the neuronal function deficit in the MCAO model rats. As evidenced by the immunochemical staining, BrdU(+)/DCX(+), BrdU(+)/nestin(+), and BrdU(+) vascular endothelial cells were promoted to proliferate in SVZ after tongxinluo administration. The matured neurons stained by NeuN and vascularization by laminin staining were observed after tongxinluo administration in the peri-infarct area. Conclusion. Tongxinluo postischemia administration could ameliorate the neurological function deficit in the model rats. Possible mechanisms are related to neurogenesis and angiogenesis in the peri-infarct area and SVZ.

Effect of the Chinese traditional prescription Suo Quan Wan on TRPV1 expression in the bladder of rats with bladder outlet obstruction.

BACKGROUND: Suo Quan Wan (SQW) is a Chinese traditional prescription that has been used in clinical treatment of lower urinary tract symptoms for centuries. However, scientific basis of SQW efficacy and mechanism is still needed. This study investigated the effect of SQW on bladder function and transient receptor potential vanilloid 1 (TRPV1) expression in the bladder of rats with bladder outlet obstruction (BOO). The induced changes in bladder function in overactive bladder (OAB) rat model were observed following different periods of outlet obstruction to obtain an appropriate rat model. METHODS: This study was carried out in two parts. In the first part, female Sprague-Dawley rats received sham operations or partial BOO operations. Two, four, and six weeks later, the OAB model groups and control were subjected to urodynamic tests to measure differences in bladder functions. Once the appropriate rat model was obtained, the second part of the experiment was performed. The rat model was recreated and treated with SQW. Urodynamic assessment was conducted, and the bladders of the rats were then removed. Immunofluorescence staining, real-time PCR, and Western blot were performed to localize and quantify the expression of TRPV1 in the bladder. RESULTS: Results of the first part indicated that at 2 and 4 weeks, the OAB model group exhibited significant differences in urodynamic parameters, including bladder pressure, maximum voiding pressure, and maximum bladder capacity, compared with the sham group. At 4 and 6 weeks, the OAB model group exhibited significant differences in residual volume (RV) and non-voiding contraction frequency. Six-week OAB model group showed much more RV but less voiding efficiency when compared with 6-week sham group or 2-and 4-week OAB model group. Rats that underwent BOO exhibited similarities with the compensated state before four weeks and may have entered decompensated state at six weeks. Studies conducted with 4-week OAB model were appropriate. In part two of the experiment, unstable bladder in the OAB model group recovered bladder stability after SQW treatment, accompanied by improved bladder hypertrophy, as well as corrected urodynamic parameters. Expression of TRPV1 mRNA and proteins in the bladder was significantly greater in the OAB model group than that in the control group, which subsequently decreased significantly with SQW treatment in BOO-induced rats. CONCLUSIONS: SQW can modulate the expression of TRPV1 in accordance with the recovery of bladder function.

Intracerebroventricular injection of epidermal growth factor reduces neurological deficit and infarct volume and enhances nestin expression following focal cerebral infarction in adult hypertensive rats.

1. Studies have documented the proliferative effects of epidermal growth factor (EGF) on neural progenitor cells in the normal or injured brain. The effect of EGF on post-stroke cerebral expression of nestin, a marker of neural progenitor cells, has not been examined in hypertensive rats. 2. In the present study, adult renovascular hypertensive Sprague-Dawley rats underwent either real or sham middle cerebral artery occlusion (MCAO). Intracerebroventricular injections of either 1 microg EGF or vehicle (0.01 mol/L phosphate-buffered saline containing 0.1 mg/mL rat serum albumin) were made 24 and 48 h after MCAO. Then, 1, 2, 3 and 4 weeks after MCAO, the postural reflex was evaluated in a blinded fashion before rat brains were processed to determine the infarct volume plus immunoreactivity for nestin and/or glial fibrillary acidic protein (GFAP). Another group of rats was used to quantify nestin expression using western blot analysis. 3. Middle cerebral artery occlusion resulted in a focal infarct that was largest at 1 week and diminished gradually over the time. The impaired postural reflex followed a similar time-course. In addition, MCAO induced a marked increase in nestin expression in both hemispheres, with a higher expression in the right hemisphere; this change was maximal at 1 week and largely subsided at 3 or 4 weeks. Within the right hemisphere, nestin expression was most pronounced in the subventricular and peri-infarct zones. Most nestin-immunoreactive cells were also positive for GFAP. 4. Thus, EGF treatment significantly increases nestin expression, reduces infarct volume and ameliorates postural reflex impairment in adult hypertensive rats.

Ebselen attenuates oxidative DNA damage and enhances its repair activity in the thalamus after focal cortical infarction in hypertensive rats.

Oxidative DNA damage has been proposed to be a major contributor to focal cerebral ischemic injury. However, little is known about the role of oxidative DNA damage in remote damage secondary to the primary infarction. In the present study, we investigated oxidative damage within the ventroposterior nucleus (VPN) after distal middle cerebral artery occlusion (MCAO) in hypertensive rats. We also examined the possible protective effect of ebselen, one glutathione peroxidase mimic, on delayed degeneration in the VPN after distal MCAO. Neuronal damage in the ipsilateral VPN was examined by Nissl staining. Oxidative DNA damage and base repair enzyme activity were assessed by analyzing immunoreactivity of 8-hydroxy-2'-deoxyguanosine (8-ohdG) and 8-oxoguanine DNA glycosylase (OGG1), respectively. The number of intact neurons in the ipsilateral VPN decreased by 52% compared to the contralateral side in ischemia group 2 weeks after distal cerebral cortical infarction. The immunoreactivity of 8-ohdG significantly increased while OGG1 immunoreactivity significantly decreased in the ipsilateral VPN 2 weeks after distal cortical infarction (all p<0.01). Compared with vehicle treatment, ebselen significantly attenuated the neuron loss, ameliorated ischemia-induced increase in 8-ohdG level as well as decrease in OGG1 level within the ipsilateral VPN (all p<0.01). OGG1 was further demonstrated to mainly express in neurons. These findings strongly suggest that oxidative DNA damage may be involved in the delayed neuronal death in the VPN region following distal MCAO. Furthermore, ebselen protects against the delayed damage in the VPN when given at 24 h following distal MCAO.

Nogo-A is involved in secondary axonal degeneration of thalamus in hypertensive rats with focal cortical infarction.

We investigate whether Nogo-A is involved in the secondary axonal degeneration in the thalamus after distal middle cerebral artery occlusion (MCAO) in stroke-prone renovascular hypertensive rats (RHRSP). The expression of Nogo-A in ipsilateral ventroposterior nucleus (VPN) of the thalamus in RHRSP was observed at 1, 2 and 4 weeks after distal MCAO. In addition, intracerebroventricular infusion of NEP1-40, a Nogo-66 receptor (NgR) antagonist peptide, was administered starting 24 h after MCAO and continued for 1, 2 and 4 weeks, respectively. Axonal damage and regeneration were evaluated by analysis of the immunoreactivity (IR) of amyloid betaA4 precursor protein (APP), growth associated protein 43 (GAP-43) and microtubule associated protein 2 (MAP-2) in ipsilateral VPN of the thalamus at 1, 2 and 4 weeks after distal MCAO. Following ischemia, the expression of Nogo-A in oligodendrocytes increased persistently and its localization became redistributed around damaged axons and dendrites. Administration of NEP1-40 downregulated the expression of Nogo-A, reduced axonal injury and enhanced axonal regeneration. Our data suggest that Nogo-A is involved in secondary axonal degeneration and that inhibition of Nogo-A can reduce neuronal damage in the thalamus after distal MCAO.