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1. Anti-inflammatory and anti-apoptotic effects of Zc3h12d against cerebral ischemia‒reperfusion through the modulation of the NF-κB signaling pathway

Author

Lijia Peng, Wenya Bai, Junjie Li, Li Xiong, Siying Huo, and Jianlin Shao

Subjects
Zc3h12d, Cerebral ischemia‒reperfusion, Inflammation, Apoptosis, Nf-κb, Neurology. Diseases of the nervous system, RC346-429
Abstract

Objective: Anti-inflammatory and anti-apoptotic therapy is expected to become the focus for attenuating cerebral ischemia‒reperfusion injury (CIRI), but the underlying mechanism needs to be further elucidated. Zc3h12d has been reported to downregulate NF-κB signaling pathway. Nevertheless, no studies have been conducted to investigate whether Zc3h12d is associated with the development of CIRI. The aim of this study was to investigate whether Zc3h12d can ameliorate CIRI and the underlying mechanism. Methods: MCAO/R and OGD/R were performed to mimic CIRI in vitro and in vivo, respectively. The expression levels of Zc3h12d, proinflammatory cytokines, proapoptotic protein, and p-p65 were detected by RT‒qPCR, ELISA or Western blotting assays. Immunofluorescence staining was used to detect the spatial distribution of Zc3h12d and the expression of p-p65 in the nucleus. Apoptotic analyses were performed by TUNEL staining, Nissl staining and flow cytometry. Cell viability was assessed using the CCK-8 assay. Results: CIRI increased Zc3h12d expression and neuronal apoptosis in the brain. Zc3h12d was predominantly located in neurons in the cortex. Overexpression of Zc3h12d can inhibit inflammation and suppress neuronal apoptosis in cells after CIRI. Furthermore, overexpression of Zc3h12d decreased the expression of p-p65 in the nucleus, which was attenuated by TNF-α, a common NF-κB agonist. In addition, overexpression of Zc3h12d can also shorten the half-life of proinflammatory cytokines. Conclusion: Zc3h12d may play a crucial role in inhibiting inflammation and apoptosis after CIRI, and the underlying mechanism may be related to repressing the activation of NF-κB signaling. Targeting Zc3h12d may be a novel strategy for preventing CIRI.

Published
2024
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2. The Minimum Effective Concentration (MEC95) of different volumes of ropivacaine for ultrasound-guided caudal epidural block: a dose-finding study

Author

Dongmei Ma, Yan Chen, Ping Chen, Jianhong Xu, Jian Guo, and Lijia Peng

Subjects
Caudal epidural block, Ultrasound, Dixon up-and-down method, Anesthesiology, RD78.3-87.3
Abstract

Abstract Background Caudal epidural block (CEB) may be beneficial in anorectal surgery because its use may extend postoperative analgesia. This dose-finding study aimed to estimate the minimum effective anesthetic concentrations for 95% patients(MEC95) of 20 ml or 25 ml of ropivacaine in with CEB. Patients and methods In this double-blind, prospective study, the concentration of ropivacaine administered in 20 ml and 25 ml for ultrasound-guided CEB were determined using the sample up-and-down sequential allocation study design of binary response variables. The first participant was given 0.5% ropivacaine. Depending on whether a block was successful or unsuccessful, the concentration of local anesthesia was decreased or increased by 0.025% in the next patient. Every five minutes for 30 min, the sensory blockade using a pin-prick sensation at S3 dermatome compared to at T6 dermatome were evaluated every 5 min within 30 min. An effective CEB was defined as a a reduction of sensation at S3 dermatome and the existence of flaccid anal sphincter. Anesthesia was considered successful if the surgeon could perform the surgery without additional anesthesia. We determined the MEC50 using the Dixon and Massey up-and-down method and estimated the MEC95 using probit regression. Results The concentration of ropivacaine administered in 20 ml for CEB ranged from 0.2% to 0.5%. Probit regression with a bias-corrected Morris 95% CI derived by bootstrapping showed an MEC50 and MEC 50 of ropivacaine for anorectal surgical anesthesia were 0.27% (95% CI, 0.24 to 0.31) and 0.36%(95% CI, 0.32 to 0.61). The concentration of ropivacaine administered in 25 ml for CEB ranged from 0.175 to 0.5. Probit regression with a bias-corrected Morris 95% CI derived by bootstrapping showed an MEC50 and MEC95 for CEB were 0.24% (95% CI, 0.19 to 0.27) and 0.32% (95% CI, 0.28 to 0.54). Conclusion With ultrasound-guided CEB, the MEC95 of 0.36% ropivacaine at 20 ml and 0.32% ropivacaine at 25 ml provide adequate surgical anesthesia/analgesia 95% of patients undergoing anorectoal surgery. Trial registration Clinicaltrails.gov: Retrospectively registered (ChiCTR2100042954; Registration date:1/2, 2021).

Published
2023
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3. Dual-branch Branch Networks Based on Contrastive Learning for Long-Tailed Remote Sensing.

Author

Lei Zhang, Lijia Peng, Pengfei Xia, Chuyuan Wei, Chengwei Yang, and Yanyan Zhang

Subjects
DEEP learning, IMAGE recognition (Computer vision), DISTANCE education, IMAGE representation, REMOTE sensing, PROBLEM solving
Abstract

Deep learning has been widely used in remote sensing image classification and achieves many excellent results. These methods are all based on relatively balanced data sets. However, in real-world scenarios, many data sets belong to the long-tailed distribution, resulting in poor performance. In view of the good performance of contrastive learning in long-tailed image classification, a new dualbranch fusion learning classification model is proposed to fuse the discriminative features of remote sensing images with spatial data, making full use of valuable image representation information in imbalance data. This paper also presents a hybrid loss, which solves the problem of poor discrimination of extracted features caused by large intra-class variation and inter-class ambiguity. Extended experiments on three long-tailed remote sensing image classification data sets demonstrate the advantages of the proposed dual-branch model based on contrastive learning in long-tailed image classification. [ABSTRACT FROM AUTHOR]

Published
2024
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4. The FGFR1 Signaling Pathway Upregulates the Oncogenic Transcription Factor FOXQ1 to Promote Breast Cancer Cell Growth

Author

Yan Lin, Fengkang Lin, Zhuoran Zhang, Lijia Peng, Wenli Yang, Mao Yang, Bo Luo, Ting Wu, Dabing Li, Xuesen Li, Bing Ran, Songyot Anuchapreeda, Rujirek Chaiwongsa, Pinyaphat Khamphikham, Suwit Duangmano, Jianming Xu, Tao He, and Sakorn Pornprasert

Subjects
Cell Biology, Molecular Biology, Applied Microbiology and Biotechnology, Ecology, Evolution, Behavior and Systematics, Developmental Biology
Published
2023

6. Biliverdin Protects Against Cerebral Ischemia/Reperfusion Injury by Regulating the miR-27a-3p/Rgs1 Axis

Author

Junjie Li, Wenya Bai, Wei Yang, Jianlin Shao, Peihua Peng, Lijia Peng, and Wendong Chen

Subjects
Neuropsychiatric Disease and Treatment, Rgs1, Inflammation, Neuroprotection, cerebral ischemia/reperfusion, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Downregulation and upregulation, medicine, Viability assay, Original Research, Biliverdin, TUNEL assay, business.industry, apoptosis, biliverdin, medicine.disease, Molecular biology, 030227 psychiatry, chemistry, Apoptosis, inflammation, medicine.symptom, business, Reperfusion injury, 030217 neurology & neurosurgery, miR-27a-3p
Abstract

Junjie Li,* Lijia Peng,* Wenya Bai, Peihua Peng, Wendong Chen, Wei Yang, Jianlin Shao Department of Anesthesiology, First Affiliated Hospital, Kunming Medical University, Kunming City, 650032, People’s Republic of China*These authors contributed equally to this workCorrespondence: Jianlin ShaoDepartment of Anesthesiology, First Affiliated Hospital of Kunming Medical University, 295 Xichang Road, Wuhua, Kunming, Yunnan, 650000, People’s Republic of ChinaTel +86-871-6532488-2755Email cmushaojlmz@163.comBackground: We have previously demonstrated that biliverdin has neuroprotective effects that ameliorate cerebral ischemia/reperfusion (I/R) injury in rats. However, the underlying mechanism is unknown. This study aimed at elucidating on the modulatory role of miR-27a-3p on Rgs1 as a mechanism by which biliverdin affects cerebral I/R injury.Methods: Middle cerebral artery occlusion/reperfusion (MCAO/R) was used to establish I/R rat models while oxygen glucose deprivation/reoxygenation (OGD/R) was used to induce hippocampal neurons to establish I/R models in vitro. Infarct volume was assessed by TTC staining. Apoptotic analyses of ischemic cortical neurons and cells were performed by TUNEL staining and flow cytometry, respectively. Cell viability was assessed by the CCK-8 assay while the target of miR-27a-3p was determined by double luciferase reporter assay. Relative expression levels of miR-27a-3p and Rgs1 (in vivo and in vitro) as well as markers of inflammation and apoptosis (in vitro) were detected by RT-qPCR. Then, Elisa and western blot were used to assess protein expression levels of inflammatory and apoptotic markers in vitro.Results: Biliverdin suppressed inflammation and apoptosis in hippocampal neurons upon OGD/R, and reduced cerebral infarction volume as well as apoptosis in the MCAO/R rat model. Furthermore, biliverdin upregulated miR-27a-3p and downregulated hippocampal neuron Rgs1 after OGD/R as well as in rat brain tissues after cerebral I/R. Bioinformatic analysis revealed an miR-27a-3p docking site in the 3ʹ-UTR region of Rgs1. Luciferase reporter assays showed that Rgs1 is an miR-27a-3p target. Moreover, miR-27a-3p upregulation inhibited OGD/R-triggered inflammation and suppressed neuronal apoptosis. Rgs1 knockdown suppressed OGD/R-triggered inflammation and decreased neuronal apoptosis while miR-27a-3p downregulation reversed the protective effect of Rgs1 knockdown. Moreover, miR-27a-3p overexpression and Rgs1 silencing suppressed NF-κB (p65) expression.Conclusion: Biliverdin protects against cerebral I/R injury by regulating the miR-27a-3p/Rgs1 axis, thereby inhibiting inflammation and apoptosis.Keywords: cerebral ischemia/reperfusion, biliverdin, miR-27a-3p, Rgs1, inflammation, apoptosis

Published
2021

7. MicroRNA-27a-3p relieves inflammation and neurologic impairment after cerebral ischaemia reperfusion via inhibiting lipopolysaccharide induced TNF factor and the TLR4/NF-κB pathway

Author

Jing Luo, Junjie Li, Li Xiong, Linna Fan, Lijia Peng, Yuan Yang, Di Lu, and Jianlin Shao

Subjects
Inflammation, Lipopolysaccharides, Interleukin-6, General Neuroscience, NF-kappa B, Apoptosis, Cerebral Infarction, Phosphoproteins, Brain Ischemia, Rats, Toll-Like Receptor 4, MicroRNAs, Reperfusion, Animals, Nervous System Diseases
Abstract

Cerebral ischaemia reperfusion (CIR) affects microRNA (miR) expression and causes substantial inflammation. Here, we investigated the influence and underlying mechanism of miR-27a-3p in rats with CIR. First, biliverdin treatment relieved cerebral infarction and decreased the levels of serum interleukin (IL)-1β, IL-6, and TNF-α. Through our previous study, we found key miR-27a-3p and its targeted gene LITAF might involve in the molecular mechanism of CIR. Then, the regulation between miR-27a-3p and LITAF was verified by the temporal miR-27a-3p and LITAF expression profiles and luciferase assay. Moreover, intracerebroventricular injection of the miR-27a-3p mimic significantly decreased the LITAF, TLR4, NF-κB, and IL-6 levels at 24 h post-surgery, whereas miR-27a-3p inhibitor reversed these effects. Furthermore, miR-27a-3p mimic could relieve cerebral infarct and neurologic deficit after CIR. In addition, injection of miR-27a-3p mimic decreased neuronal damage induced by CIR. Taken together, our results suggest that miR-27a-3p protects against CIR by relieving inflammation, neuronal damage, and neurologic deficit via regulating LITAF and the TLR4/NF-κB pathway.

Published
2022

9. MicroRNA-27a-3p Relives Inflammation and Neurologic Impairment after Cerebral Ischemia Reperfusion via Inhibiting LITAF and the TLR4/NF-κB Pathway

Author

Fan Linna, Di Lu, Lijia Peng, Li Xiong, Junjie Li, Yang Yuan, Jianlin Shao, and Jing Luo

Subjects
business.industry, Microrna 27a, Tlr4 nf κb, Cancer research, Ischemia, Medicine, Inflammation, medicine.symptom, business, medicine.disease
Abstract

Background: Cerebral ischemia reperfusion (CIR) affects microRNA (miR) expression and causes substantial inflammation. Here, we investigated the influence and underlying mechanism of miR-27-3p in rats with CIR.Methods: Cerebral ischemia reperfusion was built by tMCAO. Rats were randomly divided into Sham group, brain ischemic reperfusion (IR) group, brain ischemic reperfusion transfected with NC group, brain ischemic reperfusion transfected with miR-27a-3p mimic group, brain ischemic reperfusion transfected with miR-27a-3p inhibitor group and brain ischemic reperfusion transfected with miR-27a-3p mimic and Litaf mimic group. The relationship between miR-27a-3p and Litaf was verified via qRT-PCR and luciferase assays. The cellular distribution of Litaf was determined via double immunofluorescence. The effect of miR-27a-3p on the expression of Litaf, TLR4, NF-κB and IL-6 was evaluated using synthetic miR-27a-3p mimic and inhibitor. The level of Nissl’s body in each group was detected by Nissl’s staining. The infarct in each group was evaluated by TTC staining.Results: Firstly, BV treatment relieves cerebral infarction and decreases the levels of serum IL-1β, IL-6 and TNF-α. Through our previous study, we found key microRNA mR-27a-3p and its targeted gene Litaf might involve in the molecular mechanism of CIR. Then, the regulation between miR-27a-3p and Litaf was verified by the temporal miR-27a-3p and Litaf expression profiles and luciferase assay. Moreover, intracerebroventricular injection of the miR-27a-3p mimic significantly decreased the Litaf, TLR4, NF-κB and interleukin (IL)-6 levels and the double-labeled cell count 24 h post-surgery, whereas miR-27a-3p inhibitor reversed these effects. Furthermore, miR-27a-3p mimic could relive cerebral infarct and neurologic deficit after CIR. In addition, injection of miR-27a-3p mimic decreased neuronal damage induced by CIR.Conclusions: Increasing miR-27-3p levels protect against CIR by relieving inflammation, neuronal damage and neurologic deficit by inhibiting LITAF and the TLR4/NF-κB pathway.

Published
2020

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