Current research status and reflection on acupuncture treatment for brain disorders. / é’ˆç¸æ²»ç–—è„‘ç— çš„ç ”ç©¶çŽ°çŠ¶ä¸Žæ€è€ƒ.

Acupuncture has demonstrated positive efficacy in the treatment of brain disorders. However, significant challenges lie in integrating acupuncture with modern technologies, promoting its clinical application in treating brain disorders, elucidating the mechanisms underlying acupuncture's preventive and therapeutic effects on brain disorders, and accelerating the pace of translational development in acupuncture medicine. This paper briefly outlines the current research status, challenges, and potential future directions in acupuncture treatment for brain disorders, aiming to provide essential insights for the modernization and development of acupuncture in the treatment of brain disorders.

Electroacupuncture-modulated extracellular ATP levels in prefrontal cortex ameliorated depressive-like behavior of maternal separation rats.

Maternal separation (MS) is a type of early-life stress that has been linked to neuropsychiatric disorders, especially depression. Increasing evidence indicates that the adenosine triphosphate (ATP) level in the prefrontal cortex (PFC) is involved in the pathophysiology of depression. To investigate the potential relationship between ATP in PFC and antidepressant effects of electroacupuncture (EA) treatment, we assessed genes involved in ATP biosynthesis as well as the extracellular ATP levels in a rat model exposed to neonatal MS. Our results demonstrated that reduced expression of ABCG2 (an ATP-binding cassette protein) and ATP levels in the PFC of depressive-like rats exposed to MS can be attenuated by EA stimulus at the Baihui (GV20) and Yintang (GV29) acupoints. Moreover, the antidepressant effect of EA treatment was blocked by administration of suramin, a broad purinergic P2 receptor antagonist. Together, these results suggested that electroacupuncture may be able to modulate extracellular ATP levels in the PFC of depressive-like MS rats, potentially contributing to its antidepressant effects.

Organized Resting-state Functional Dysconnectivity of the Prefrontal Cortex in Patients with Schizophrenia.

Schizophrenia has prominent functional dysconnectivity, especially in the prefrontal cortex (PFC). However, it is unclear whether in the same group of patients with schizophrenia, PFC functional dysconnectivity appears in an organized manner or is stochastically located in different subregions. By investigating the resting-state functional connectivity (rsFC) of each PFC subregion from the Brainnetome atlas in 40 schizophrenia patients and 40 healthy subjects, we found 24 altered connections in schizophrenia, and the connections were divided into four categories by a clustering analysis: increased connections within the PFC, increased connections between the inferior PFC and the thalamus/striatum, reduced connections between the PFC and the motor control areas, and reduced connections between the orbital PFC and the emotional perception regions. In addition, the four categories of rsFC showed distinct cognitive engagement patterns. Our findings suggest that PFC subregions have specific functional dysconnectivity patterns in schizophrenia and may reflect heterogeneous symptoms and cognitive deficits in schizophrenia.

Taurine inhibits neuron apoptosis in hippocampus of diabetic rats and high glucose exposed HT-22 cells via the NGF-Akt/Bad pathway.

Type 2 Diabetes causes learning and memory deficits that might be mediated by hippocampus neuron apoptosis. Studies found that taurine might improve cognitive deficits under diabetic condition because of its ability to prevent hippocampus neuron apoptosis. However, the effect and mechanism is not clear. In this study, we explore the effect and mechanism of taurine on inhibiting hippocampus neuron apoptosis. Sixty male Sprague-Dawley rats were randomly divided into control, T2D, taurine treatment (giving 0.5%, 1%, and 2% taurine in drinking water) groups. Streptozotocin was used to establish the diabetes model. HT-22 cell (hippocampus neurons line) was used for in vitro experiments. Morris Water Maze test was used to check the learning and memory ability, TUNEL assay was used to measure apoptosis and nerve growth factor (NGF); Akt/Bad pathway relevant protein was detected by western blot. Taurine improved learning and memory ability and significantly decreased apoptosis of the hippocampus neurons in T2D rats. Moreover, taurine supplement also inhibited high glucose-induced apoptosis in HT-22 cell in vitro. Mechanistically, taurine increased the expression of NGF, phosphorylation of Trka, Akt, and Bad, as well as reduced cytochrome c release from mitochondria to cytosol. However, beneficial effects of taurine were blocked in the presence of anti-NGF antibody or Akt inhibitor. Taurine could inhibit hippocampus neuron apoptosis via NGF-Akt/Bad pathway. These results provide some clues that taurine might be efficient and feasible candidate for improvement of learning and memory ability in T2D rats.

Taurine Promotes Neuritic Growth of Dorsal Root Ganglion Cells Exposed to High Glucose in Vitro.

Diabetic neuropathy (DN) is the most common chronic complication of DM and its major pathological changes show axonal dysfunction, atrophy and loss. However, there are few reports that taurine promotes neurite growth of dorsal root ganglion (DRG) cells. In current study, DRG neurons were exposed to high glucose (HG) with or without taurine. The neurite outgrowth of DRG neurons was observed by fluorescent immunohistochemistry method. Expression of Gap-43, Akt, phosphorylated Akt, mTOR and phosphorylated mTOR was determined by Western blot assay. Our results showed that HG significantly decreased the neurite outgrowth and expression of Gap-43 in DRG neurons. Moreover, phosphorylated levels of Akt and mTOR were downregulated in DRG neurons exposed to HG. On the contrary, taurine supplementation significantly reversed the decreased neurite outgrowth and Gap-43 expression, and the downregulated phosphorylated levels of Akt and mTOR. However, the protective effects of taurine were blocked in the presence of PI3K antagonists LY294002 or Akt antagonists Perifosine. These results indicate that taurine promotes neurite outgrowth of DRG neurons exposed to HG via activating Akt/mTOR signal pathway.

Taurine protects against myelin damage of sciatic nerve in diabetic peripheral neuropathy rats by controlling apoptosis of schwann cells via NGF/Akt/GSK3ß pathway.

Diabetic peripheral neuropathy is a common complications of Type 2 Diabetes and its main pathological feature is myelin sheath damage of peripheral nerve that was induced by Schwann cells (SCs) apoptosis. Increasing evidence suggested that taurine might play a role in improving DPN because of its ability to prevent SCs apoptosis. In this study, we explore the effect of taurine on preventing SCs apoptosis and its underlying mechanism. Sprague Dawley rats were treated with streptozotocin to establish the diabetes model. Rats were randomly divided into control, diabetes, taurine treatment (as giving 0.5%, 1% and 2% taurine in drinking water) groups. RSC96 cell (a rat SCs line) was used for intervention experiments in vitro. Results showed that taurine significantly corrected morphology of damaged myelin sheath and inhibited SCs apoptosis in sciatic nerve of diabetic rats. Moreover, taurine prevented apoptosis of RSC96 cells exposed to high glucose. Mechanistically, taurine up-regulated NGF expression and phosphorylation levels of Akt and GSK3ß, while, blocking activation of NGF and phosphorylation of Akt and GSK3ß increased apoptosis of high glucose-exposed RSC96 cells with taurine supplement. These results revealed taurine improved the myelin sheath damage of sciatic nerve in diabetic rats by controlling SCs apoptosis via NGF/Akt/GSK3ß signaling pathways, which provides some clues that taurine might be effective and feasible candidate for the treatment of DPN.

An evaluation of nutrition intervention during radiation therapy in patients with locoregionally advanced nasopharyngeal carcinoma.

PURPOSE: To evaluate the effectiveness of nutrition intervention during radiation for patients with locoregionally advanced (III-IVa) nasopharyngeal carcinoma (NPC). MATERIALS AND METHODS: We retrospectively reviewed 117 patients with locoregionally advanced (III-IVa) NPC treated between December 2015 and March 2016 in Zhejiang Cancer Hospital. All the patients underwent radical chemo-radiotherapy. First, all the patients were divided into the nutrition intervention group and the control group, depending on whether they accepted nutrition intervention. Repeated measures were used to analyze the change of nutritional indicators before, during, and after radiation therapy and to simultaneously compare the difference in nutritional status between the two groups at the same time point. Subsequently, the 117 patients were divided into the malnourished group (weight loss > 5%) and the non-malnourished group (weight loss ≤ 5%) according to whether their weight loss was over 5% of their body weight during radiotherapy. Chi-square tests and logistic regression analysis were used to explore the influence factors for the weight loss. RESULTS: The repeated measures showed that all indicators including weight, body mass index (BMI), albumin, pre-albumin(PA), and prognostic nutritional index (PNI) dramatically declined in both groups compared with their levels before radiation therapy (All p < 0.001). However, there was no significant difference between the intervention and non-intervention groups regarding the mean values of nutritional indicators at the same time point, that before, during, and after radiation therapy, except BMI (All p > 0.05). Logistic regression analysis revealed grade ≥ 3 radiation-induced oral mucositis as the prognostic factor for a poor nutrition status (odds ratio, OR = 3.232, p = 0.021, confidence interval, CI [1.198, 8.820]). Besides this, patients with a decrease of >15% in pre-albumin level were more likely to be malnourished (OR = 2.442, p = 0.041, CI [1.036, 5.757]). Similar to that observed in our former analysis, we did not find that existing nutrition intervention can significantly improve nutritional status (OR = 1.217, p = 0.704, CI [0.042, 3.348]). CONCLUSIONS: Our study shows that the nutritional status of the patients gradually declined during treatment. We concluded that grade ≥ 3 radiation-induced oral mucositis would aggravate the extent of malnutrition during radiation therapy in patients with locoregionally advanced NPC. Pre-albumin level was a predictive marker for weight loss in patients with NPC. However, current nutrition intervention during radiation therapy can't significantly reverse nutritional status.