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      Drug Design, Development and Therapy (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on the design and development of drugs, as well as the clinical outcomes, patient safety, and programs targeted at the effective and safe use of medicines. Sign up for email alerts here.

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      Rutaecarpine may improve neuronal injury, inhibits apoptosis, inflammation and oxidative stress by regulating the expression of ERK1/2 and Nrf2/HO-1 pathway in rats with cerebral ischemia-reperfusion injury

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          Abstract

          Background

          Cerebral ischemia-reperfusion (CI/R) injury is a more serious brain injury caused by the recovery of blood supply after cerebral ischemia for a certain period of time. Rutaecarpine (Rut) is an alkaloid isolated from Evodia officinalis with various biological activities. Previous studies have shown that Rut has a certain protective effect on ischemic brain injury, but the specific molecular mechanism is still unknown.

          Methods

          In this study, a rat model of CI/R was established to explore the effects and potential molecular mechanisms of Rut on CI/R injury in rats.

          Results

          The results showed that Rut alleviated neuronal injury induced by CI/R in a dose-dependent manner. Besides, Rut inhibited neuronal apoptosis by inhibiting the activation of caspase 3 and the expression of Bax. In addition, Rut alleviated the inflammatory response and oxidative stress caused by CI/R through inhibiting the production of pro-inflammatory factors (IL-6 and IL-1β), lactate dehydrogenase (LDH), malondialdehyde (MDA) and ROS, and increased the levels of anti-inflammatory factors (IL-4 and IL-10) and superoxide dismutase (SOD). Biochemically, Western blot analyses showed that Rut inhibited the phosphorylation of ERK1/2 and promoted the expression of nuclear factor-erythroid 2 related factor 2 (Nrf2) pathway-related proteins (Nrf2, heme oxygenase 1 (HO-1) and NAD (P) H-quinone oxidoreductase 1) in a dose-dependent manner. These results show that Rut may alleviate brain injury induced by CI/R by regulating the expression of ERK1/2 and the activation of Nrf2/HO-1 pathway.

          Conclusion

          In conclusion, these results suggest that Rut may be used as an effective therapeutic agent for damage caused by CI/R.

          Most cited references36

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          Neurogenesis following Stroke Affecting the Adult Brain.

          Olle Lindvall, Zaal Kokaia (2015)
          A bulk of experimental evidence supports the idea that the stroke-damaged adult brain makes an attempt to repair itself by producing new neurons also in areas where neurogenesis does not normally occur (e.g., the striatum and cerebral cortex). Knowledge about mechanisms regulating the different steps of neurogenesis after stroke is rapidly increasing but still incomplete. The functional consequences of stroke-induced neurogenesis and the level of integration of the new neurons into existing neural circuitries are poorly understood. To have a substantial impact on the recovery after stroke, this potential mechanism for self-repair needs to be enhanced, primarily by increasing the survival and differentiation of the generated neuroblasts. Moreover, for efficient repair, optimization of neurogenesis most likely needs to be combined with promotion of other endogenous neuroregenerative responses (e.g., protection and sprouting of remaining mature neurons, transplantation of neural stem/progenitor cells [NSPC]-derived neurons and glia cells, and modulation of inflammation).
          Article 0 comments Cited 79 times – based on 0 reviews     Review now
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            Protective Effects and Target Network Analysis of Ginsenoside Rg1 in Cerebral Ischemia and Reperfusion Injury: A Comprehensive Overview of Experimental Studies

            Weijie Xie, Ping Zhou, Yifan Sun … (2018)
            Cerebral ischemia-reperfusion is a complicated pathological process. The injury and cascade reactions caused by cerebral ischemia and reperfusion are characterized by high mortality, high recurrence, and high disability. However, only a limited number of antithrombotic drugs, such as recombinant tissue plasminogen activator (r-TPA), aspirin, and heparin, are currently available for ischemic stroke, and its safety concerns is inevitable which associated with reperfusion injury and hemorrhage. Therefore, it is necessary to further explore and examine some potential neuroprotective agents with treatment for cerebral ischemia and reperfusion injury to reduce safety concerns caused by antithrombotic drugs in ischemic stroke. Ginseng Rg1 (G-Rg1) is a saponin composed of natural active ingredients and derived from the roots or stems of Panax notoginseng and ginseng in traditional Chinese medicine. Its pharmacological effects exert remarkable neurotrophic and neuroprotective effects in the central nervous system. To explore and summarize the protective effects and mechanisms of ginsenoside Rg1 against cerebral ischemia and reperfusion injury, we conducted this review, in which we searched the PubMed database to obtain and organize studies concerning the pharmacological effects and mechanisms of ginsenoside Rg1 against cerebral ischemia and reperfusion injury. This study provides a valuable reference and clues for the development of new agents to combat ischemic stroke. Our summarized review and analysis show that the pharmacological effects of and mechanisms underlying ginsenoside Rg1 activity against cerebral ischemia and reperfusion injury mainly involve 4 sets of mechanisms: anti-oxidant activity and associated apoptosis via the Akt, Nrf2/HO-1, PPARγ/HO-1, extracellular regulated protein kinases (ERK), p38, and c-Jun N-terminal kinase (JNK) pathways (or mitochondrial apoptosis pathway) and the caspase-3/ROCK1/MLC pathway; anti-inflammatory and immune stimulatory-related activities that involve apoptosis or necrosis via MAPK pathways (the JNK1/2 + ERK1/2 and PPARγ/HO-1 pathways), endoplasmic reticulum stress (ERS), high mobility group protein1 (HMGB1)-induced TLR2/4/9 and receptor for advanced glycation end products (RAGE) pathways, and the activation of NF-κB; neurological cell cycle, proliferation, differentiation, and regeneration via the MAPK pathways (JNK1/2 + ERK1/2, PI3K-Akt/mTOR, PKB/Akt and HIF-1α/VEGF pathways); and energy metabolism and the regulation of cellular ATP levels, the blood-brain barrier and other effects via N-methyl-D-aspartic acid (NMDA) receptors, ERS, and AMP/AMPK-GLUT pathways. Collectively, these mechanisms result in significant neuroprotective effects against cerebral ischemic injury. These findings will be valuable in that they should further promote the development of candidate drugs and provide more information to support the application of previous findings in stroke clinical trials.
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              Heme oxygenase-1 as a target for drug discovery.

              Roberto Motterlini, Roberta Foresti (2014)
              Heme oxygenase enzymes, which exist as constitutive (HO-2) and inducible (HO-1) isoforms, degrade heme to carbon monoxide (CO) and the bile pigment biliverdin. In the last two decades, substantial scientific evidence has been collected on the function of HO-1 in cell homeostasis, emphasizing these two important features: (i) HO-1 is a fundamental "sensor" of cellular stress and directly contributes toward limiting or preventing tissue damage; (ii) the products of HO-1 activity dynamically participate in cellular adaptation to stress and are inherently involved in the mechanisms of defence.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Drug Des Devel Ther
                Journal ID (iso-abbrev): Drug Des Devel Ther
                Journal ID (publisher-id): DDDT
                Journal ID (pmc): dddt
                Title: Drug Design, Development and Therapy
                Publisher: Dove
                ISSN (Electronic): 1177-8881
                Publication date (Electronic): 20 August 2019
                Publication date Collection: 2019
                Volume: 13
                Pages: 2923-2931
                Affiliations
                [1 ]Department of Internal Medicine, The Second People’s Hospital of Dongying City , Dongying City, Shandong Province 257335, People’s Republic of China
                [2 ]Department of Critical Care Medicine ICU, Zoucheng People’s Hospital , Zoucheng, Shandong Province 273500, People’s Republic of China
                [3 ]Department of Internal Neurology, Shanghai Pudong Hospital, Fudan University Pudong Medical Center , Pudong, Shanghai 201399, People’s Republic of China
                Author notes
                Correspondence: Yang ChenDepartment of Internal Neurology, Shanghai Pudong Hospital, Fudan University Pudong Medical Center , 2800 Gongwei Road, Huinan Town, Pudong, Shanghai201399, People’s Republic of ChinaTel +86 1 356 895 4215Email l8nz03s78@sina.com
                [*]

                These authors contributed equally to this work

                Article
                Publisher ID: 216156
                DOI: 10.2147/DDDT.S216156
                PMC ID: 6708397
                PubMed ID: 31692511
                SO-VID: b5f0e0d3-f678-47c5-8f00-9cd98b7439a2
                Copyright © © 2019 Han et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 17 May 2019
                Date accepted : 31 July 2019
                Page count
                Figures: 5, References: 38, Pages: 9
                Categories
                Subject: Original Research

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: cerebral ischemia-reperfusion,rutaecarpine,nuclear factor-erythroid 2 related factor 2,extracellular regulated protein kinases
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Keywords: cerebral ischemia-reperfusion, rutaecarpine, nuclear factor-erythroid 2 related factor 2, extracellular regulated protein kinases

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