Effects of rhodioloside on the neurological functions of rats with total cerebral ischemia/reperfusion and cone neuron injury in the hippocampal CA1 region

Zhang, Yue; Xia-zhen, Guo; Wang, Guohua; Liu, Jidan; Liang, Peiyu; Wang, Huan; Zhu, Chunyan; Wu, Qiong

doi:10.7717/peerj.10056

Cited by 14 publications

(23 citation statements)

References 28 publications

(26 reference statements)

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“…It was demonstrated that the expression of ISG15 was also reduced by epidermal growth factor (EGF), which suggested the expression of ISG15 could be reduced by EGF-induced miR-223. The apoptotic rate was measured by flow cytometry and the expressions of anti-apoptotic Bcl-2 ( Bruckheimer et al, 1998 ), and pro-apoptotic caspase 3 ( Choudhary et al, 2015 ) and p53 ( Aubrey et al, 2018 ; Zhang et al, 2020a , 2021a ; Niu et al, 2021a , b ) were detected to evaluate the apoptosis of gMEC. The inflammation of gMEC was estimated by inflammation-related proteins.…”

Section: Discussionmentioning

confidence: 99%

EGF-Induced miR-223 Modulates Goat Mammary Epithelial Cell Apoptosis and Inflammation via ISG15

Zhang

Niu

et al. 2021

Front. Cell Dev. Biol.

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The health of mammary gland is essential for lactation. Epidermal growth factor (EGF) is reported to play an important role in lactation initiation and miR-223 is a conserved microRNA in anti-inflammation. In this study, EGF was found to induce a higher expression of miR-223 in goat mammary epithelial cell (gMEC). The downstream genes of miR-223 were screened by RNA sequencing, including Interferon-stimulated gene product 15 (ISG15), a pivotal immune responder, which was detected to be downregulated by EGF and miR-223. Due to the correlation between inflammation and apoptosis, the gMEC apoptosis modulated by EGF, miR-223, and ISG15 was investigated, and the protein expressions of Bcl-2/Bax, Caspase 3 and p53 were examined to evaluate the apoptosis of gMEC. The protein expressions of p-STAT3/STAT3, PR, FOXC1, and HOXA10, which had been shown to be related to inflammation, were detected to assess the inflammation of gMEC. This study provided a regulation axis, EGF/miR-223/ISG15, and illustrated its regulation to gMEC apoptosis and inflammation.

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Section: Discussionmentioning

confidence: 99%

EGF-Induced miR-223 Modulates Goat Mammary Epithelial Cell Apoptosis and Inflammation via ISG15

Zhang

Niu

et al. 2021

Front. Cell Dev. Biol.

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“…After going through the remaining full-text articles, 120 articles were excluded for at least one of following reasons: 1) the article was not a research about ischemic stroke; 2) not an in vivo study; 3) the intervention was a combination of RRC with potential effect on ischemic stroke; 4) the study did not access the effects of RRC on the animal model of ischemic stroke; 5) no control group. Finally, 15 eligible studies (Chen et al, 2009; Shi et al, 2012;Chen et al, 2014;Yu et al, 2014;Han et al, 2015;Atochin et al, 2016;Chen et al, 2016;Liu et al, 2018;Zhang et al, 2018;Zuo et al, 2018;Zhong et al, 2019;Li et al, 2020;Zhang et al, 2020;Dong et al, 2021) involving 345 animals were identified (Figure 1).…”

Section: Study Inclusionmentioning

confidence: 99%

“…Three studies used C57BL/6 mice (n 67). The weight of rats ranged from 190 to 320 g, and the weight of mice ranged from 18 to 23 g. Cerebral ischemic injury in the included studies was induced by temporary middle cerebral artery occlusion (MCAO) in which ischemic time varied from 8 to 180 min (Chen et al, 2009;Shi et al, 2012;Chen et al, 2014;Yu et al, 2014;Han et al, 2015;Atochin et al, 2016;Liu et al, 2018;Zhang et al, 2018;Zuo et al, 2018;Zhong et al, 2019;Li et al, 2020;Zhang et al, 2020;Dong et al, 2021), and permanent MCAO (Chen et al, 2016). For anesthesia chosen in experiments, four studies (Shi et al, 2012;Han et al, 2015;Atochin et al, 2016;Zhang et al, 2020) used chloral hydrate, three studies (Zuo et al, 2018;Zhong et al, 2019) used isoflurane, four studies (Chen et al, 2016;Zhang et al, 2018;Li et al, 2020;Dong et al, 2021) used sodium pentobarbital, and the remaining four studies (Chen et al, 2009;Chen et al, 2014;Yu et al, 2014;Liu et al, 2018) did not report it.…”

Section: Characteristics Of Included Studiesmentioning

confidence: 99%

“…The weight of rats ranged from 190 to 320 g, and the weight of mice ranged from 18 to 23 g. Cerebral ischemic injury in the included studies was induced by temporary middle cerebral artery occlusion (MCAO) in which ischemic time varied from 8 to 180 min (Chen et al, 2009;Shi et al, 2012;Chen et al, 2014;Yu et al, 2014;Han et al, 2015;Atochin et al, 2016;Liu et al, 2018;Zhang et al, 2018;Zuo et al, 2018;Zhong et al, 2019;Li et al, 2020;Zhang et al, 2020;Dong et al, 2021), and permanent MCAO (Chen et al, 2016). For anesthesia chosen in experiments, four studies (Shi et al, 2012;Han et al, 2015;Atochin et al, 2016;Zhang et al, 2020) used chloral hydrate, three studies (Zuo et al, 2018;Zhong et al, 2019) used isoflurane, four studies (Chen et al, 2016;Zhang et al, 2018;Li et al, 2020;Dong et al, 2021) used sodium pentobarbital, and the remaining four studies (Chen et al, 2009;Chen et al, 2014;Yu et al, 2014;Liu et al, 2018) did not report it. Ten studies utilized a dose gradient of RRC: one study (Atochin et al, 2016) used 5, 10 and 20 mg kg −1 intravenously, one study (Chen et al, 2016) used 20, and 40 mg kg −1 orally, one study (Han et al, 2015) used 15, and 30 mg kg −1 intraperitoneally, one study (Liu et al, 2018) used 2.5, 5, 10 and 20 mg kg −1 intravenously, two studies (Zhang et al, 2018;Li et al, 2020) used 25, 50 and 100 mg kg −1 intraperitoneally, one study used 20, 50 and 100 mg kg −1 intraperitoneally, one study …”

Section: Characteristics Of Included Studiesmentioning

confidence: 99%

“…For anesthesia chosen in experiments, four studies (Shi et al, 2012;Han et al, 2015;Atochin et al, 2016;Zhang et al, 2020) used chloral hydrate, three studies (Zuo et al, 2018;Zhong et al, 2019) used isoflurane, four studies (Chen et al, 2016;Zhang et al, 2018;Li et al, 2020;Dong et al, 2021) used sodium pentobarbital, and the remaining four studies (Chen et al, 2009;Chen et al, 2014;Yu et al, 2014;Liu et al, 2018) did not report it. Ten studies utilized a dose gradient of RRC: one study (Atochin et al, 2016) used 5, 10 and 20 mg kg −1 intravenously, one study (Chen et al, 2016) used 20, and 40 mg kg −1 orally, one study (Han et al, 2015) used 15, and 30 mg kg −1 intraperitoneally, one study (Liu et al, 2018) used 2.5, 5, 10 and 20 mg kg −1 intravenously, two studies (Zhang et al, 2018;Li et al, 2020) used 25, 50 and 100 mg kg −1 intraperitoneally, one study used 20, 50 and 100 mg kg −1 intraperitoneally, one study (Zhong et al, 2019) used 20, 40, and 80 mg kg −1 intraperitoneally, one study (Zuo et al, 2018) used 10, 20, and 40 mg kg −1 intraperitoneally, and one study (Zhang et al, 2020) used 12 and 48 mg kg −1 through gavage. Six studies (Shi et al, 2012;Chen et al, 2014;Atochin et al, 2016;Chen et al, 2016;Zuo et al, 2018;Zhong et al, 2019) administrated RRC before stroke; Seven studies (Shi et al, 2012;Yu et al, 2014;Chen et al, 2016;Liu et al, 2018;Zhang et al, 2018;…”

Section: Characteristics Of Included Studiesmentioning

confidence: 99%

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Preclinical Evidence and Possible Mechanisms of Rhodiola rosea L. and Its Components for Ischemic Stroke: A Systematic Review and Meta-Analysis

Cai

Mao

et al. 2021

Front. Pharmacol.

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Background:Rhodiola rosea L. has long been used as traditional medicines in Europe and Asia to treat a variety of common conditions and diseases including Alzheimer’s disease, cardiovascular disease, cognitive dysfunctions, cancer, and stroke. Previous studies reported that Rhodiola rosea L. and its components (RRC) improve ischemia stroke in animal models. Here, we conducted a systematic review and meta-analysis for preclinical studies to evaluate the effects of RRC and the probable neuroprotective mechanisms in ischemic stroke.Methods: Studies of RRC on ischemic stroke animal models were searched in seven databases from inception to Oct 2021. The primary measured outcomes included the neural functional deficit score (NFS), infarct volume (IV), brain water content, cell viability, apoptotic cells, terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL)-positive cells, B-cell lymphoma-2 (Bcl-2) level and tumor necrosis factor-α (TNF-α) level. The secondary outcome measures were possible mechanisms of RRC for ischemic stroke. All the data were analyzed via RevMan version 5.3.Results: 15 studies involving 345 animals were identified. Methodological quality for each included studies was accessed according to the CAMARADES 10-item checklist. The quality score of studies range from 1 to 7, and the median was 5.53. Pooled preclinical data showed that compared with the controls, RRC could improve NFS (Zea Longa (p < 0.01), modified neurological severity score (mNSS) (p < 0.01), rotarod tests (p < 0.01), IV (p < 0.01), as well as brain edema (p < 0.01). It also can increase cell viability (p < 0.01), Bcl-2 level (p < 0.01) and reduce TNF-α level (p < 0.01), TUNEL-positive cells (p < 0.01), apoptotic cells (p < 0.01).Conclusion: The findings suggested that RRC can improve ischemia stroke. The possible mechanisms of RRC are largely through antioxidant, anti-apoptosis activities, anti-inflammatory, repressing lipid peroxidation, antigliosis, and alleviating the pathological blood brain barrier damage.

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Pharmacological effects of salidroside on central nervous system diseases

Jin

Wang

et al. 2022

Biomedicine & Pharmacotherapy

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Effects of rhodioloside on the neurological functions of rats with total cerebral ischemia/reperfusion and cone neuron injury in the hippocampal CA1 region

Cited by 14 publications

References 28 publications

EGF-Induced miR-223 Modulates Goat Mammary Epithelial Cell Apoptosis and Inflammation via ISG15

EGF-Induced miR-223 Modulates Goat Mammary Epithelial Cell Apoptosis and Inflammation via ISG15

Preclinical Evidence and Possible Mechanisms of Rhodiola rosea L. and Its Components for Ischemic Stroke: A Systematic Review and Meta-Analysis

Pharmacological effects of salidroside on central nervous system diseases

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