Protective Effect of Compound Tongluo Decoction on Brain Vascular Endothelial Cells after Ischemia-Reperfusion by Inhibition of Ferroptosis Through Regulating Nrf2/ARE/SLC7A11 Signaling Pathway.

Cerebral infarction is one of the most common diseases for aged people. Compound Tongluo Decoction (CTLD), a classic traditional Chinese Medicine prescription, has been widely used in the treatment of ischemic cerebral infarction. Transient middle cerebral artery occlusion (tMCAO) rat model is established for the animal experiment and oxygen-glucose deprivation and reperfusion (OGD/R) human umbilical vein endothelial cells (HUVECs) model are established for the cell experiment. This also use Nrf2-/- rats to detect the role of nuclear factor erythroid 2-related factor 2 (Nrf2). Longa score, Evans blue staining, brain water content measurement, and histological observation are done. The levels of reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), and other ferroptosis-related components are detected respectively. In the vivo experiment, CTLD relieved ischemia-reperfusion (IR) injury symptoms and attenuated IR injury in brain tissues of tMCAO rats by relieving peroxidation injury in brain tissues and inhibiting ferroptosis in tMCAO rats. Moreover, CTLD reversed OGD/R-induced oxidative damage of endothelial cells via suppressing ferroptosis. After knocking out the Nrf2 gene, the protective effect of CTLD is sharply reduced. This study put forward that CTLD can inhibit ferroptosis in I/R-injured vascular endothelium by regulating Nrf2/ARE/SLC7A11 signaling to improve the relative symptoms of rats after cerebral I/R injury, thus providing a viable treatment option for cerebrovascular disease.

Transcriptome sequencing and network pharmacology-based approach to reveal the effect and mechanism of Ji Chuan Jian against Parkinson's disease.

BACKGROUND: Ji Chuan Jian (JCJ), a classic Traditional Chinese Medicine (TCM) formula, has been widely applied in treating Parkinson's disease (PD) in China, However, the interaction of bioactive compounds from JCJ with the targets involved in PD remains elusive. METHODS: Based on the transcriptome sequencing and network pharmacology approaches, the chemical compounds of JCJ and gene targets for treating PD were identified. Then, the Protein-protein interaction (PPI) and "Compound-Disease-Target" (C-D-T) network were constructed by using of Cytoscape. Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were applied to these target proteins. Finally, AutoDock Vina was used for applying molecular docking. RESULTS: In the present study, a total number of 2669 differentially expressed genes (DEGs) were identified between PD and healthy controls using whole transcriptome RNA sequencing. Then, 260 targets of 38 bioactive compounds in JCJ were identified. Of these targets, 47 were considered PD-related targets. Based on the PPI degree, the top 10 targets were identified. In C-D-T network analysis, the most important anti-PD bioactive compounds in JCJ were determined. Molecular docking revealed that potential PD-related targets, matrix metalloproteinases-9 (MMP9) were more stably bound with naringenin, quercetin, baicalein, kaempferol and wogonin. CONCLUSION: Our study preliminarily investigated the bioactive compounds, key targets, and potential molecular mechanism of JCJ against PD. It also provided a promising approach for identifying the bioactive compounds in TCM as well as a scientific basis for further elucidating the mechanism of TCM formulae in treating diseases.

Compound Tongluo Decoction inhibits endoplasmic reticulum stress-induced ferroptosis and promoted angiogenesis by activating the Sonic Hedgehog pathway in cerebral infarction.

ETHNOPHARMACOLOGICAL RELEVANCE: Cerebral infarction is one of the most common types of cerebrovascular diseases that threaten people's health. Compound Tongluo Decoction (CTLD), a traditional Chinese medicine formula, has various pharmacological activities, including the alleviation of cerebral infarction symptoms. AIM OF THE STUDY: This study aims to explore the potential mechanism by which CTLD alleviates cerebral infarction. MATERIAL AND METHODS: Middle cerebral artery occlusion (MCAO) rat model and oxygen-glucose deprivation and reperfusion (OGD/R) cell model were established for research. The expression of proteins related to endoplasmic reticulum (ER) stress, ferroptosis, Sonic Hedgehog (SHH) pathway and angiogenesis was analyzed by Western blot analysis. The expression of CD31 was detected by immunofluorescence to investigate angiogenesis. In addition, the expression of GRP78 and XBP-1 in brain tissues was investigated by immunohistochemistry. With the application of Prussian blue staining, iron deposition in brain tissue was detected. The levels of reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) were detected using ELISA kits. The angiogenesis was analyzed by tube formation assay. RESULTS: The results presented in this research showed that CTLD and 4-phenyl butyric acid (4-PBA; the inhibitor of ER stress) could alleviate cerebral infarction. Mechanistically, CTLD and 4-PBA rescued ER stress and ferroptosis, but promoted SHH signaling in rats with cerebral infarction. In addition, cerebral infarction exhibited a high level of angiogenesis, which was aggravated by CTLD but suppressed by 4-PBA. Furthermore, CTLD inhibited ER stress and ferroptosis, but promoted SHH signaling and angiogenesis in OGD/R-induced PC12 cells, which was partly abolished by SANT-1, an antagonist of SHH signaling. CONCLUSION: In conclusion, this study revealed that CTLD might inhibit ferroptosis induced by endoplasmic reticulum stress and promote angiogenesis by activating the Sonic Hedgehog pathway in rats with cerebral infarction.

UHPLC-MS-based metabolomics and chemoinformatics study reveals the neuroprotective effect and chemical characteristic in Parkinson's disease mice after oral administration of Wen-Shen-Yang-Gan decoction.

Parkinson's disease (PD), the typical neurodegenerative disease, is characterized by the progressive loss of dopaminergic neurons in the substantia nigra (SN). However, no therapeutic agent used currently could slow down neuronal cell loss so as to decelerate or halt the progression of PD. Traditional Chinese medicine (TCM) has been utilized to treat the dysfunction of the autonomic nervous system. Wen-Shen-Yang-Gan decoction (WSYGD) has a good effect on the clinical treatment of PD with constipation. However, it is not clear which ingredients and what mechanism are responsible for the therapeutic effect. In this study, the pharmacodynamic study of WSYGD in PD mice was applied. Concurrently, a novel method for the identification of metabolic profiles of WSYGD has been developed. Finally, we found that WSYGD could protect the PD mice induced by rotenone. The underlying mechanism of the protective effect may be related to the reduction of the DA neurons apoptosis via reducing inflammatory reaction. By virtue of UPLC-MS and chemoinformatics method, 35 prototype compounds and 27 metabolites were filtered out and tentatively characterized. In conclusion, this study provides an insight into the metabolism of WSYGD in vivo to enable understanding of the metabolic process and therapeutic mechanism of PD.

Effect of Wenshen-Yanggan Decoction on Movement Disorder and Substantia Nigra Dopaminergic Neurons in Mice with Chronic Parkinson's Disease.

This study aimed to explore the protective effects of Wenshen-Yanggan decoction on dopaminergic (DA) neuron injury in a rotenone-induced mouse model with chronic Parkinson's disease (PD) and explore its mechanism of action. Ultraperformance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) was used to measure the content of six main components in the Wenshen-Yanggan decoction. The chronic PD mouse model was established by treating 10-month-old healthy wild C57BL/6 male mice with rotenone 30 mg/kg/day for 28 days in succession. The pole test and rotarod test were applied to detect the rescue effect of Wenshen-Yanggan decoction in high, medium, and low dosages, respectively, on PD-like behaviors in mice with chronic PD. The protective effect of Wenshen-Yanggan decoction on the mesencephalic nigrostriatal DA neuron injury was determined employing tyrosine hydroxylase (TH) immunofluorescence staining. Enzyme-linked immunosorbent assay (ELISA) was adopted to measure the inflammatory cytokines in serum, including TNF-α (tumor necrosis factor-alpha), IFN-γ (interferon gamma), NF-κB (nuclear factor kappa-B), and IL-1ß (interleukin-1 beta). Western blotting was performed to quantify the expression of phosphorylated c-Jun N-terminal kinase (p-JNK), cleaved caspase-3, B-cell lymphoma-2 (Bcl-2), and NF-κB in the brain. Our results showed that the Wenshen-Yanggan decoction in high, medium, and low dosages reduced the turning time of mice (P < 0.01, P < 0.01, and P < 0.05). The high and medium dosages shortened the total climbing time of PD mice in the pole test (P < 0.01 and P < 0.05). Meanwhile, the high, medium, and low dosages increased the rod-standing time of PD mice in the rotarod test (P < 0.01, P < 0.05, and P < 0.05). Besides, the decoction reversed the decrease in TH-positive neurons induced by rotenone, upregulated TH protein expression, and downregulated the α-syn expression in the PD model. Moreover, the decoction in high dosage significantly inhibited the expression of p-JNK, cleaved caspase-3, and NF-κB in the midbrain of PD mice (P < 0.05, P < 0.05, and P < 0.01), upregulated the expression of Bcl-2 (P < 0.05), and decreased the content of TNF-α, IFN-γ, NF-κB, and IL-1ß in the serum (P < 0.001, P < 0.001, P < 0.001, and P < 0.001). Taken together, the Wenshen-Yanggan decoction could protect mice from rotenone-induced chronic PD, which might be related to the reduction of the DA neuron apoptosis via suppressing the inflammatory reaction and the neuronal apoptosis pathway.

Sheng-Di-Da-Huang Decoction Inhibited Inflammation Expressed in Microglia after Intracerebral Hemorrhage in Rats.

OBJECTS: Sheng-Di-Da-Huang Decoction was used as an effective hemostatic agent in ancient China. However, its therapeutic mechanism is still not clear. Inflammatory injury plays a critical role in ICH-induced secondary brain injury. After hemolysis, hematoma components are released, inducing microglial activation via TLR4, which initiates the activation of transcription factors (such as NF-κB) to regulate expression of proinflammatory cytokine genes. This study aimed to verify the anti-inflammatory effects of Sheng-Di-Da-Huang Decoction on ICH rats. MATERIALS AND METHODS: Intracerebral hemorrhage was induced by injection of bacterial collagenase (0.2 U) in rats. Neurological deficits, brain water content, Evans blue extravasation, expression of TLR4, NF-κB, Iba-1 positive cells (activated microglia), tumor necrosis factor-α (TNF-α), and interleukin-1ß (IL-1ß) were examined 1, 3, 7, and 14 days after collagenase injection. MR images were also studied. RESULTS: Sheng-Di-Da-Huang Decoction remarkably improved neurological function, reduced brain water content as well as Evans blue extravasation, downregulated expression of TLR4, NF-κB, TNF-α, and IL-1ß, and inhibited microglial activation. CONCLUSIONS: Sheng-Di-Da-Huang Decoction reduced inflammation reaction after ICH through inhibited inflammation expressed in microglia.

Jia-Jian-Di-Huang-Yin-Zi decoction exerts neuroprotective effects on dopaminergic neurons and their microenvironment.

As a classical prescription of Traditional Chinese medicine, the Jia-Jian-Di-Huang-Yin-Zi (JJDHYZ) decoction has long been used to treat movement disorders. The present study evaluated the effects of JJDHYZ on dopaminergic (DA) neurons and their survival-enhancing microenvironment as well as the possible mechanisms involved using a mouse model of Parkinson's disease. In MPTP-lesioned mice, a high dosage of JJDHYZ (34 g/kg/day) attenuated the loss of DA neurons, reversed the dopamine depletion, and improved the expression of glial-derived neurotrophic factor (GDNF) compared to the untreated model group. JJDHYZ also protected the ultrastructure of the blood-brain barrier (BBB) and tight junction proteins by inhibiting the activation of microglia and astrocytes besides the increase in three types of matrix metalloproteinases in the substantia nigra. In conclusion, the JJDHYZ-high dosage (JJDHYZ-H) group exhibited the neuroprotection of DA neurons, and the underlying mechanism may be related to the survival-enhancing microenvironment of the DA neurons.

Apocynum venetum Leaf Extract Exerts Antidepressant-Like Effects and Inhibits Hippocampal and Cortical Apoptosis of Rats Exposed to Chronic Unpredictable Mild Stress.

We investigated the effects of Apocynum venetum leaf extract (AVLE) on depressive behaviors and neuronal apoptosis in a chronic unpredictable mild stress (CUMS) rat model of depression. Rats were randomly divided into six groups: control, chronic unpredictable mild stress, fluoxetine, AVLE30, AVLE60, and AVLE120. Except for the control group, all rats were submitted to chronic unpredictable mild stress paradigms for four weeks to induce depressive behavior. Neuronal apoptosis was assessed by the terminal deoxynucleotidyl transferase- (TDT-) mediated dUTP-biotin nick end-labeling (TUNEL) method. The expression levels of apoptosis-related proteins, such as B-cell lymphoma 2 (Bcl-2), Bcl-2 Associated X Protein (Bax), cysteine-aspartic acid protease-3 and protease-9 (caspase-3 and caspase-9), cytochrome c (cyt-C), brain-derived neurotrophic factor (BDNF), and cAMP-response element binding (CREB) protein, were evaluated by western blot. Treatment with AVLE (60 or 120 mg/kg/day) significantly improved depressive behavior. Increased apoptosis of hippocampus and cortical neurons were observed in CUMS rats, while 120 mg/kg/day of AVLE significantly reversed these changes and achieved the best antidepressant-like effects among the doses tested. Moreover, AVLE (120 mg/kg) significantly increased Bcl-2, BDNF, and CREB protein expression and decreased Bax, cyt-C, and caspase family protein expression. Our results indicate that AVLE has potent antidepressant activity, likely due to its ability to suppress neuronal apoptosis.

Apocynum venetum leaf extract reverses depressive-like behaviors in chronically stressed rats by inhibiting oxidative stress and apoptosis.

BACKGROUND: Major depressive disorder (MDD) is a common but serious psychiatric disorder, but current treatments are inadequate for approximately half of the patients with MDD. Thus, better methods of treatment are urgently needed. This study aimed to investigate the antidepressant-like effects and potential mechanism of Apocynum venetum leaf extract (AVLE) in chronic unpredictable mild stress (CUMS) rat model of depression. MATERIALS AND METHODS: The CUMS rat model of depression was used to investigate the antidepressant-like activity and relevant mechanism of AVLE (30, 60, and 125 mg/kg, i.g.). Behavioral tests, including sucrose preference test (SPT), open field test (OFT), and forced swimming test (FST) were conducted to assess anhedonic, despairing, and spontaneous behaviors, respectively. The activity of the hypothalamic-pituitary-adrenal (HPA) axis was evaluated by measuring the serum adrenocorticotrophic hormone (ACTH) and corticosterone (CORT) concentrations. The underlying mechanism was further explored by assessing oxidative stress parameters, cell apoptosis, and brain-derived neurotrophic factor (BDNF) expression in the rat hippocampus exposed to CUMS. RESULTS: The AVLE (36, 60, 125 mg/kg) treatment exerted antidepressant-like effects in CUMS-exposed rats similar to fluoxetine (10 mg/kg). The AVLE treatment reduced the serum CORT and ACTH levels in CUMS rats. It also increased the activities and gene expression of antioxidant enzymes (SOD, CAT, and GPx) and decreased the ROS generation levels and the lipid peroxidation marker MDA in the rat hippocampus subjected to CUMS. Additionally, it suppressed the apoptosis of hippocampus cells by modulating Bcl-2/Bax pathways and improved the hippocampal BDNF expressions of CUMS rats. CONCLUSION: Our findings suggested that AVLE exerted antidepressant-like effects in CUMS rats, which was possibly mediated by the prevention of oxidative stress, the inhibition of hippocampal neuronal apoptosis, and the upregulation of the hippocampal BDNF level.

Jia-Jian-Di-Huang-Yin-Zi decoction reduces apoptosis induced by both mitochondrial and endoplasmic reticulum caspase12 pathways in the mouse model of Parkinson's disease.

ETHNOPHARMACOLOGICAL RELEVANCE: As a classical prescription of traditional Chinese medicine (TCM), Jia-Jian-Di-Huang-Yin-Zi decoction (JJDHYZ) has been used to treat the symptoms of neurological disorders with a long history. AIM OF THE STUDY: To evaluate the effects and possible mechanisms of JJDHYZ on a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced subacute mouse model of Parkinson's disease. MATERIALS AND METHODS: Adult male C57BL/6 mice were randomly divided into five groups: control, MPTP, JJDHYZ low dosage (JJDHYZ-L, 8.5g/kg/day), medium dosage (JJDHYZ-M, 17g/kg/day) and high dosage (JJDHYZ-H, 34g/kg/day). Behavioral tests, immunohistochemistry, immunofluorescence, and high-performance liquid chromatography (HPLC) were conducted to evaluate the neuroprotective effects of JJDHYZ. The mechanism was further explored using TdT-mediated dUTP nick end labeling staining and transmission electron microscopy. The protein expression of Bax, Bcl-2, cytochrome c, full-length caspase9, cleaved caspase9, cleaved caspase3, caspase12 and C/EBP homologous protein was assessed. The toxicity on hepatocytes and renal cells was detected using the enzyme-linked immunosorbent assay kits. RESULTS: JJDHYZ-H restored the behavior performance impaired by MPTP, and reduced the loss of tyrosine hydroxylase. Additionally, it blocked the apoptosis, activated cleaved caspase3 and protected the ultrastructural integrity of mitochondria by regulating the expression of proteins in both mitochondrial and endoplasmic reticulum (ER) caspase12 pathways. CONCLUSIONS: JJDHYZ-H showed behavior recovery and dopamine neuron protection by inhibiting the apoptotic activities associated with mitochondrial and ER caspase12 pathways.

Synergic Effect of Borneol and Ligustrazine on the Neuroprotection in Global Cerebral Ischemia/Reperfusion Injury: A Region-Specificity Study.

The cooperation of ligustrazine (LI) and borneol was proved to be much better than each of them in treating cerebral ischemia. However, the mechanism of their synergic therapy is unclear till now. Moreover, whether their cooperation brought different degrees of protection among different brain regions was also unclear. In the present study, the effects of LI, borneol, and their mixture were observed in global cerebral ischemia-reperfusion (GCIR) injury by detecting microcirculation, expressions of caspase-3 and p53, levels of IL-1ß, IL-6, and TNF-α, and contents of SOD, GSH-Px, and MDA in cortex, hippocampus, hypothalamus, and striatum, respectively. Furthermore, Nissl bodies were scored also. Monotherapy of LI or borneol showed obvious improvements in the four regions, specially in cortex and hippocampus. Interestingly, the cooperation of LI and borneol brought some new improvements, specially in hypothalamus and striatum. Thus, the synergic effect of the two drugs showed region-specificity in GCIR injury except the expressions of caspase-3 and p53.

PI3K/Akt pathway contributes to neuroprotective effect of Tongxinluo against focal cerebral ischemia and reperfusion injury in rats.

ETHNOPHARMACOLOGICAL RELEVANCE: Tongxinluo (TXL), a compound prescription, is formulated according to the collateral disease doctrine of traditional Chinese medicine, and is widely used for the treatment of cardio-cerebrovascular diseases in China. AIM OF THE STUDY: We aimed to investigate the neuroprotective effect of TXL on focal cerebral ischemia and reperfusion injury in rats by attenuating its brain damage and neuronal apoptosis, and to assess the potential role of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway in this protection. MATERIALS AND METHODS: Adult Male Sprague-Dawley rats (n=120) were randomly divided into 5 groups: sham, cerebral ischemia and reperfusion (I/R), cerebral ischemia and reperfusion plus TXL (1.6g/kg/day) (TXL1.6), TXL1.6 plus LY294002 and dimethyl sulfoxide (DMSO) (TXL1.6+LY294002), TXL1.6 plus DMSO (TXL1.6+vehicle). Prior to the grouping, TXL1.6 was selected to be the optimal dose of TXL by evaluating the neurological deficits score of five group rats (Sham, I/R, TXL0.4, TXL0.8 and TXL1.6, n=30) at 0, 1, 3, 5, and 7 days after reperfusion. Rats, being subjected to middle cerebral artery occlusion (MCAO) for 90min followed by 24h reperfusion, were the cerebral ischemia/reperfusion models. At 24h after reperfusion, cerebral infarct area was measured via tetrazolium staining and neuronal damage was showed by Nissl staining. The double staining of Terminal deoxynucleotidyl transferase-mediated deoxyuridine 5-triphosphate nick end labeling (TUNEL) staining and immunofluorescence labeling with NeuN, was performed to evaluate neuronal apoptosis. Proteins involved in PI3K/Akt pathway were detected by Western blot. RESULTS: The results showed that TXL markedly improved neurological function, reduced cerebral infarct area, decreased neuronal damage, and significantly attenuated neuronal apoptosis, while these effects were eliminated by inhibition of PI3K/Akt with LY294002. We also found that TXL up-regulated the expression levels of p-PDK1, p-Akt, p-c-Raf, p-BAD and down-regulated Cleaved caspase 3 expression notably, which were partially reversed by LY294002. Additionally, the increment of p-PTEN level on which LY294002 had little effect was also detected in response to TXL treatment. CONCLUSIONS: These findings demonstrated that TXL provided neuroprotection against cerebral ischemia/reperfusion injury and neuronal apoptosis, and this effect was mediated partly by activation of the PI3K/Akt pathway.

Tongxinluo reduces brain edema and inhibits post-ischemic inflammation after middle cerebral artery occlusion in rats.

ETHNOPHARMACOLOGICAL RELEVANCE: Tongxinluo (TXL), a widely used traditional Chinese medicine, has been proved multiple therapeutic effects in cerebral ischemic infraction. The purpose of this study was to investigate the protective effects of TXL on the brain edema and post-ischemic inflammatory response. MATERIALS AND METHODS: Middle cerebral artery occlusion in the rat was used as the ischemia model. Rats were treated with TXL. In the first stage, the best dosage was chosen based on functional assessment and infarct size. In the second stage, rats were randomly divided into 5 groups: sham control (sham), ischemia and reperfusion (IR) 24h, TXL24h, I/R72h, TXL72h. TXL(1.6g/kg/day) administration was pre-performed for 3 days in TXL groups, and was post-performed for 24h (TXL24h group) or 72h (TXL72h group). Brain edema was measured by water content, MRI and AQP4 expression. Iba1, HMGB1, TLR4, NF-κB expression were examined by immunofluorescence staining or Western blot. TNF-α was determined by enzyme-linked immunosorbent assay. RESULTS: High dose (1.6g/kg/day) of TXL remarkably reduced neurological deficit scores and cerebral infarct area. Compared with those results of I/R24h group, pre-post treatment with TXL for 3 days decreased brain water content, down-regulated AQP4 expression, lowered relative signal intensity of T2WI, reduced lesion volume ratio, and inhibited the activation of microglia, HMGB1, TLR4, NF-κB and TNF-α. CONCLUSIONS: These results indicated that the TXL pre-post treatment for 3 days could be an effective therapy for brain ischemia by inhibiting the development of brain edema and post-ischemic inflammation.

[Effects of Tongnao Huoluo acupuncture therapy on Caspase-3 and Bcl-2 of rats with acute cerebral infarction].

OBJECTIVE: To evaluate effects of Tongnao Huoluo acupuncture therapy (THAT) on Bcl-2 and Caspase-3 rats with acute cerebral infarction (ACI). METHODS: Totally 264 SD rats were randomly divided into 5 groups, i.e. the THAT group (n =72), the thrombolysis group (n =72), the body acupuncture group (n =72), the ischemia control group (n =24), and the sham-operation group (n =24). Successfully modeled rats were recruited in all groups except the sham-operation group. Rats in the THAT group, the thrombolysis group, and the body acupuncture group were divided into 3 subgroups according to the disease occurrence time, i.e., < or = 1.5 h THAT group, 1.5+ -2 h THAT group, and 2+ -3 h THAT group. The neuroethological scores were assessed at 6, 24, and 72 h after treatment. The expressions of Bcl-2 and Caspase-3 were detected using immunohistochemical staining at 24 and 72 h respectively. RESULTS: In aspect of improving scores of neurological functions: At 6 h after treatment within 2 h after the disease occurrence, the neuroethological scores were lowered more obviously in the thrombolysis group than in the THAT group (P <0.05). There was statistical difference at 24 and 72 h within 2 - 3 h after the,disease occurrence between the THAT group and the thrombolysis group (P <0.05). Compared with before treatment, there was statistical difference at 24 and 72 h within 3 h after the disease occurrence (P <0. 05, P <0.01). In aspect of lowering the expression of Caspase-3 and elevating the expression of Bcl-2: There was statistical difference in lowering the expression of Caspase-3 and elevating the expression of Bcl-2 between the THAT group and the thrombolysis group at 72 h within 2 -3 after the disease occurrence (P <0.05, P < 0.01). CONCLUSION: THAT showed favorable effects in lowering neuroethological scores, lowering expression of Caspase-3, and elevating the expression of Bcl-2 of ACI rats.

[Impacts of tongnao huoluo acupuncture therapy on BI and NIHSS of patients with acute cerebral infarction].

OBJECTIVE: To evaluate the effect of Tongnao Huoluo Acupuncture (THA) therapy on acute cerebral infarction (ACI). METHODS: Adopting multi-centered, randomized and controlled method, 397 ACI patients from 10 hospitals subjected to the study were treated according to the initiating time (IT) of disease during hospitalization: the 138 patients of stage-1 with IT < or =6 h, were randomly assigned to three groups, treated respectively with THA (Group A), thrombolysis with urokinase (Group B) and Batroxobin (Group C); the 140 patients of stage-2 with IT within 6-48 h, and 119 patients of stage-3 with IT within 48 h-14 d were randomly assigned to three groups, treated respectively with THA (Group D) body acupuncture (Group E), and conventional treatment (Group F). Therapeutic effect was evaluated by NIHSS scores estimated at the day 1, 3, 7, 14, 28 and 90 of treatment, and the Barthel Index (BI) measured at day 14, 28 and 90. RESULTS: Effect in Group A was insignificantly different from that in Group B (P > 0.05), but was different from that in Group C significantly (P < 0.01). At day 90, the percentage of patients with high BI (HBI%, patients with BI >95%) was insignificantly different in Group A vs. B (P > 0.05), but was significantly different in Group A vs. C (P < 0.01). Comparisons between Group D, E and F showed that the therapeutic effect in Group D was equivalent to that in Group E (P < 0.05), but better than that in Group F (P < 0.01), and HBI% in Group D was superior than that in the other two groups (P < 0.01). CONCLUSIONS: THA therapy shows favorable effects in reducing the crippling rate and improving the living capacity of ACI patients.