Dataset Information

The therapeutic mechanism of Dengzhanxixin injection on middle cerebral artery occlusion rats based on proteomics

ABSTRACT: To explore the therapeutic mechanism, we carried out an Dengzhanxixin injection experiment with a focal brain ischemic deficit rat model and explore the target proteins using TMT-based proteomics. Method are shown as follow: 1. Animals and Grouping: The animal experiments were conducted under the direction of NIH Guidelines for the Care and Use of Laboratory Animals (NIH Publications No. 80-23, revised 1996). The procedures were approved by the Animal Care and Use Committees of Beijing Normal University, China. Adult male Sprague–Dawley rats were purchased from Beijing Vital River Laboratory Animal Technology Co., Ltd. The animals were allowed to acclimate for 7 d before the experiments. Rats were randomly divided into a sham-operated (sham) group, model group, Dengzhan-treated (Dengzhanxixin injection) group, and EDV-treated (edaravone, EDV) group. Dengzhan (0.36 mL/100 g) or EDV (0.18 mL/100 g) was intravenously injected into rats, the first drug treatments were performed immediately after the middle cerebral artery occlusion (MCAO) surgery, the subsequent ones were continually performed with the interval of 12 h, i.e. twice a day; and the drug treatments lasted for 7 d. The rats in the sham group and the model group were treated with the same volume of saline in the same way. 2. MCAO Surgery: Before surgery, rats were fasted overnight, with free access to water. Animals were anaesthetized with 3.5% chloral hydrate (350 mg/kg body weight, i.p.) and MCAO was performed. Briefly, the right common carotid artery, external carotid and internal carotid were exposed through a midline cut. A nylon filament with a heated rounded tip was inserted into the external carotid artery, and was pulled to the internal carotid artery to occlude the origin of the middle cerebral artery. Model animals were subject to 1.5 h of MCAO, and then to reperfusion achieved by a gentle withdrawal of the occluding thread. Sham-operated animals were subjected to the same procedure, except for the insertion of the filament.

ORGANISM(S): Rattus Norvegicus

SUBMITTER: Dongfeng Wei

PROVIDER: PXD026918 | iProX | Fri Jun 25 00:00:00 BST 2021

REPOSITORIES: iProX

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Publications

Dengzhanxixin Injection Ameliorates Cognitive Impairment Through a Neuroprotective Mechanism Based on Mitochondrial Preservation in Patients With Acute Ischemic Stroke.

An Haiting H Tao Wuhai W Liang Ying Y Li Peng P Li Min M Zhang Xiaxia X Chen Kewei K Wei Dongfeng D Xie Daojun D Zhang Zhanjun Z

Frontiers in pharmacology 20210830

Acute ischemic stroke (AIS) is a global health burden and cognitive impairment is one of its most serious complication. Adequate interventions for AIS may have the potential to improve cognitive outcomes. In the present study, we selected <i>Erigeron breviscapus</i> (Vaniot) Hand.-Mazz. injection (Dengzhanxixin injection, DZXI), a widely used Chinese herbal injection, in contrast to edaravone as the positive control drug to test its potential to ameliorates neurological and cognitive impairments ...[more]

PMID: 34526899

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Project description:OBJECTIVE: To analyze genome-wide changes in chondrocyte gene expression in a surgically induced model of early osteoarthritis (OA) in rats, to assess the similarity of this model to human OA, and to identify genes and mechanisms leading to OA pathogenesis. METHODS: OA was surgically induced in 5 rats by anterior cruciate ligament transection and partial medial meniscectomy. Sham surgery was performed in 5 additional animals, which were used as controls. Both groups underwent 4 weeks of forced mobilization, 3 times per week. RNA was extracted directly from articular chondrocytes in the OA (operated), contralateral, and sham-operated knees. Affymetrix GeneChip expression arrays were used to assess genome-wide changes in gene expression. Expression patterns of selected dysregulated genes, including Col2a1, Mmp13, Adamts5, Ctsc, Ptges, and Cxcr4, were validated by real-time polymerase chain reaction, immunofluorescence, or immunohistochemistry 2, 4, and 8 weeks after surgery. RESULTS: After normalization, comparison of OA and sham-operated samples showed 1,619 differentially expressed probe sets with changes in their levels of expression >/=1.5-fold, 722 with changes >/=2-fold, 135 with changes >/=4-fold, and 20 with changes of 8-fold. Dysregulated genes known to be involved in human OA included Mmp13, Adamts5, and Ptgs2, among others. Several dysregulated genes (e.g., Reln, Phex, and Ltbp2) had been identified in our earlier microarray study of hypertrophic chondrocyte differentiation. Other genes involved in cytokine and chemokine signaling, including Cxcr4 and Ccl2, were identified. Changes in gene expression were also observed in the contralateral knee, validating the sham operation as the appropriate control. CONCLUSION: Our results demonstrate that the animal model mimics gene expression changes seen in human OA, supporting the relevance of newly identified genes and pathways to early human OA. We propose new avenues for OA pathogenesis research and potential targets for novel OA treatments, including cathepsins and cytokine, chemokine, and growth factor signaling pathways, in addition to factors controlling the progression of chondrocyte differentiation. Experiment Overall Design: OA was surgically induced in 5 rats by anterior cruciate ligament transection and partial medial meniscectomy. Sham surgery was performed in 5 additional animals, which were used as controls. Both groups underwent 4 weeks of forced mobilization, 3 times per week. RNA was extracted directly from articular chondrocytes in the OA (operated), contralateral, and sham-operated knees, 28 days post-surgery. Affymetrix GeneChip expression arrays were used to assess genome-wide changes in gene expression.

Dataset Information

The therapeutic mechanism of Dengzhanxixin injection on middle cerebral artery occlusion rats based on proteomics

Publications

Dengzhanxixin Injection Ameliorates Cognitive Impairment Through a Neuroprotective Mechanism Based on Mitochondrial Preservation in Patients With Acute Ischemic Stroke.

Similar Datasets

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