a 2a ar gene Search Results


sirna duplexes targeting the rat α 2a -ar sirna gene  (Biomics Biotechnologies)
90
Biomics Biotechnologies sirna duplexes targeting the rat α 2a -ar sirna gene
Blocking <t>α</t> <t>2A</t> -AR <t>siRNA</t> reversed the protective role of Dex on OLT-induced intestinal injury in rats. (a) Representative images showing the microscopic findings of intestines stained with hematoxylin and eosin in seven groups. Bar scale, 10 μ m. (b) Chiu's scoring quantitating the intestinal mucosal damage. (c–d) Immunohistochemistry staining of CD3 (c) and CD4 (d) in intestinal issues. Red arrow: positive cells. Data are represented as the mean ± standard deviation, n = 8 for each group. S: sham-operated group; M: the model group with OLT; D1: rats that were pretreated with 10 μ g/kg before OLT; D2: rats that were pretreated with 50 μ g/kg before OLT; B1: rats that received 500 g/kg atipamezole at 40 min before receiving 50 μ g/kg Dex prior to OLT; B2: rats that received 50 g/kg ARC239 at 40 min before receiving 50 μ g/kg Dex prior to OLT; B3: rats that received 1.5 mg/kg BRL-44408 at 40 min before receiving 50 μ g/kg Dex prior to OLT. ∗ P < 0.05, compared to Group S; # P < 0.05, compared to Group M; $ P < 0.05, compared to Group D2.
Sirna Duplexes Targeting The Rat α 2a Ar Sirna Gene, supplied by Biomics Biotechnologies, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/sirna duplexes targeting the rat α 2a -ar sirna gene/product/Biomics Biotechnologies
Average 90 stars, based on 1 article reviews
sirna duplexes targeting the rat α 2a -ar sirna gene - by Bioz Stars, 2026-05
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gene encoding the human a 2a ar (uniprot c9jqd8) c-terminally truncated after residue ala 316  (Eurofins)
90
Eurofins gene encoding the human a 2a ar (uniprot c9jqd8) c-terminally truncated after residue ala 316
Blocking <t>α</t> <t>2A</t> -AR <t>siRNA</t> reversed the protective role of Dex on OLT-induced intestinal injury in rats. (a) Representative images showing the microscopic findings of intestines stained with hematoxylin and eosin in seven groups. Bar scale, 10 μ m. (b) Chiu's scoring quantitating the intestinal mucosal damage. (c–d) Immunohistochemistry staining of CD3 (c) and CD4 (d) in intestinal issues. Red arrow: positive cells. Data are represented as the mean ± standard deviation, n = 8 for each group. S: sham-operated group; M: the model group with OLT; D1: rats that were pretreated with 10 μ g/kg before OLT; D2: rats that were pretreated with 50 μ g/kg before OLT; B1: rats that received 500 g/kg atipamezole at 40 min before receiving 50 μ g/kg Dex prior to OLT; B2: rats that received 50 g/kg ARC239 at 40 min before receiving 50 μ g/kg Dex prior to OLT; B3: rats that received 1.5 mg/kg BRL-44408 at 40 min before receiving 50 μ g/kg Dex prior to OLT. ∗ P < 0.05, compared to Group S; # P < 0.05, compared to Group M; $ P < 0.05, compared to Group D2.
Gene Encoding The Human A 2a Ar (Uniprot C9jqd8) C Terminally Truncated After Residue Ala 316, supplied by Eurofins, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/gene encoding the human a 2a ar (uniprot c9jqd8) c-terminally truncated after residue ala 316/product/Eurofins
Average 90 stars, based on 1 article reviews
gene encoding the human a 2a ar (uniprot c9jqd8) c-terminally truncated after residue ala 316 - by Bioz Stars, 2026-05
90/100 stars
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a 2a ar gene  (GenScript corporation)
90
GenScript corporation a 2a ar gene
Blocking <t>α</t> <t>2A</t> -AR <t>siRNA</t> reversed the protective role of Dex on OLT-induced intestinal injury in rats. (a) Representative images showing the microscopic findings of intestines stained with hematoxylin and eosin in seven groups. Bar scale, 10 μ m. (b) Chiu's scoring quantitating the intestinal mucosal damage. (c–d) Immunohistochemistry staining of CD3 (c) and CD4 (d) in intestinal issues. Red arrow: positive cells. Data are represented as the mean ± standard deviation, n = 8 for each group. S: sham-operated group; M: the model group with OLT; D1: rats that were pretreated with 10 μ g/kg before OLT; D2: rats that were pretreated with 50 μ g/kg before OLT; B1: rats that received 500 g/kg atipamezole at 40 min before receiving 50 μ g/kg Dex prior to OLT; B2: rats that received 50 g/kg ARC239 at 40 min before receiving 50 μ g/kg Dex prior to OLT; B3: rats that received 1.5 mg/kg BRL-44408 at 40 min before receiving 50 μ g/kg Dex prior to OLT. ∗ P < 0.05, compared to Group S; # P < 0.05, compared to Group M; $ P < 0.05, compared to Group D2.
A 2a Ar Gene, supplied by GenScript corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/a 2a ar gene/product/GenScript corporation
Average 90 stars, based on 1 article reviews
a 2a ar gene - by Bioz Stars, 2026-05
90/100 stars
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mutant a 2a gene  (Charles River Laboratories)
90
Charles River Laboratories mutant a 2a gene
Blocking <t>α</t> <t>2A</t> -AR <t>siRNA</t> reversed the protective role of Dex on OLT-induced intestinal injury in rats. (a) Representative images showing the microscopic findings of intestines stained with hematoxylin and eosin in seven groups. Bar scale, 10 μ m. (b) Chiu's scoring quantitating the intestinal mucosal damage. (c–d) Immunohistochemistry staining of CD3 (c) and CD4 (d) in intestinal issues. Red arrow: positive cells. Data are represented as the mean ± standard deviation, n = 8 for each group. S: sham-operated group; M: the model group with OLT; D1: rats that were pretreated with 10 μ g/kg before OLT; D2: rats that were pretreated with 50 μ g/kg before OLT; B1: rats that received 500 g/kg atipamezole at 40 min before receiving 50 μ g/kg Dex prior to OLT; B2: rats that received 50 g/kg ARC239 at 40 min before receiving 50 μ g/kg Dex prior to OLT; B3: rats that received 1.5 mg/kg BRL-44408 at 40 min before receiving 50 μ g/kg Dex prior to OLT. ∗ P < 0.05, compared to Group S; # P < 0.05, compared to Group M; $ P < 0.05, compared to Group D2.
Mutant A 2a Gene, supplied by Charles River Laboratories, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/mutant a 2a gene/product/Charles River Laboratories
Average 90 stars, based on 1 article reviews
mutant a 2a gene - by Bioz Stars, 2026-05
90/100 stars
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Image Search Results


Blocking α 2A -AR siRNA reversed the protective role of Dex on OLT-induced intestinal injury in rats. (a) Representative images showing the microscopic findings of intestines stained with hematoxylin and eosin in seven groups. Bar scale, 10 μ m. (b) Chiu's scoring quantitating the intestinal mucosal damage. (c–d) Immunohistochemistry staining of CD3 (c) and CD4 (d) in intestinal issues. Red arrow: positive cells. Data are represented as the mean ± standard deviation, n = 8 for each group. S: sham-operated group; M: the model group with OLT; D1: rats that were pretreated with 10 μ g/kg before OLT; D2: rats that were pretreated with 50 μ g/kg before OLT; B1: rats that received 500 g/kg atipamezole at 40 min before receiving 50 μ g/kg Dex prior to OLT; B2: rats that received 50 g/kg ARC239 at 40 min before receiving 50 μ g/kg Dex prior to OLT; B3: rats that received 1.5 mg/kg BRL-44408 at 40 min before receiving 50 μ g/kg Dex prior to OLT. ∗ P < 0.05, compared to Group S; # P < 0.05, compared to Group M; $ P < 0.05, compared to Group D2.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Dexmedetomidine Attenuates Orthotopic Liver Transplantation-Induced Acute Gut Injury via α 2 -Adrenergic Receptor-Dependent Suppression of Oxidative Stress

doi: 10.1155/2019/9426368

Figure Lengend Snippet: Blocking α 2A -AR siRNA reversed the protective role of Dex on OLT-induced intestinal injury in rats. (a) Representative images showing the microscopic findings of intestines stained with hematoxylin and eosin in seven groups. Bar scale, 10 μ m. (b) Chiu's scoring quantitating the intestinal mucosal damage. (c–d) Immunohistochemistry staining of CD3 (c) and CD4 (d) in intestinal issues. Red arrow: positive cells. Data are represented as the mean ± standard deviation, n = 8 for each group. S: sham-operated group; M: the model group with OLT; D1: rats that were pretreated with 10 μ g/kg before OLT; D2: rats that were pretreated with 50 μ g/kg before OLT; B1: rats that received 500 g/kg atipamezole at 40 min before receiving 50 μ g/kg Dex prior to OLT; B2: rats that received 50 g/kg ARC239 at 40 min before receiving 50 μ g/kg Dex prior to OLT; B3: rats that received 1.5 mg/kg BRL-44408 at 40 min before receiving 50 μ g/kg Dex prior to OLT. ∗ P < 0.05, compared to Group S; # P < 0.05, compared to Group M; $ P < 0.05, compared to Group D2.

Article Snippet: The α 2A -AR siRNA duplexes (5′-CGAGCUGCAAGAUUAACGA-3′) targeting the rat α 2A -AR siRNA gene (gene ID: 25083; nucleotide accession number: NM_012739.3) were commercially obtained from Biomics (Jiangsu, China).

Techniques: Blocking Assay, Staining, Immunohistochemistry, Standard Deviation

Blocking α 2A -AR siRNA reversed the protective role of Dex on OLT-induced intestinal mucosal barrier injury in rats. (a–b) Western blotting results showing the levels of occludin (a) and ZO-1 (b) in rat intestines. (c–f) ELISA results showing the levels of serum biomarkers of intestinal mucosal barrier function, including DAO (c), LPS (d), I-FABP2 (e), and D-LA (f). Data are represented as the mean ± standard deviation, n = 8 for each group. S: sham-operated group; M: the model group with OLT; D1: rats that were pretreated with 10 μ g/kg before OLT; D2: rats that were pretreated with 50 μ g/kg before OLT; B1: rats that received 500 g/kg atipamezole at 40 min before receiving 50 μ g/kg Dex prior to OLT; B2: rats that received 50 g/kg ARC239 at 40 min before receiving 50 μ g/kg Dex prior to OLT; B3: rats that received 1.5 mg/kg BRL-44408 at 40 min before receiving 50 μ g/kg Dex prior to OLT. ∗ P < 0.05, compared to Group S; # P < 0.05, compared to Group M; $ P < 0.05, compared to Group D2.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Dexmedetomidine Attenuates Orthotopic Liver Transplantation-Induced Acute Gut Injury via α 2 -Adrenergic Receptor-Dependent Suppression of Oxidative Stress

doi: 10.1155/2019/9426368

Figure Lengend Snippet: Blocking α 2A -AR siRNA reversed the protective role of Dex on OLT-induced intestinal mucosal barrier injury in rats. (a–b) Western blotting results showing the levels of occludin (a) and ZO-1 (b) in rat intestines. (c–f) ELISA results showing the levels of serum biomarkers of intestinal mucosal barrier function, including DAO (c), LPS (d), I-FABP2 (e), and D-LA (f). Data are represented as the mean ± standard deviation, n = 8 for each group. S: sham-operated group; M: the model group with OLT; D1: rats that were pretreated with 10 μ g/kg before OLT; D2: rats that were pretreated with 50 μ g/kg before OLT; B1: rats that received 500 g/kg atipamezole at 40 min before receiving 50 μ g/kg Dex prior to OLT; B2: rats that received 50 g/kg ARC239 at 40 min before receiving 50 μ g/kg Dex prior to OLT; B3: rats that received 1.5 mg/kg BRL-44408 at 40 min before receiving 50 μ g/kg Dex prior to OLT. ∗ P < 0.05, compared to Group S; # P < 0.05, compared to Group M; $ P < 0.05, compared to Group D2.

Article Snippet: The α 2A -AR siRNA duplexes (5′-CGAGCUGCAAGAUUAACGA-3′) targeting the rat α 2A -AR siRNA gene (gene ID: 25083; nucleotide accession number: NM_012739.3) were commercially obtained from Biomics (Jiangsu, China).

Techniques: Blocking Assay, Western Blot, Enzyme-linked Immunosorbent Assay, Standard Deviation

Blocking α 2A -AR siRNA counteracted the alleviation of oxidative stress by Dex in intestines of rats with OLT. The levels of oxidant ROS (a) and antioxidants including GST α 1 (b), SOD (c), and GSH (d) were measured in rat intestines. Data are represented as the mean ± standard deviation, n = 8 for each group. S: sham-operated group; M: the model group with OLT; D1: rats that were pretreated with 10 μ g/kg before OLT; D2: rats that were pretreated with 50 μ g/kg before OLT; B1: rats that received 500 g/kg atipamezole at 40 min before receiving 50 μ g/kg Dex prior to OLT; B2: rats that received 50 g/kg ARC239 at 40 min before receiving 50 μ g/kg Dex prior to OLT; B3: rats that received 1.5 mg/kg BRL-44408 at 40 min before receiving 50 μ g/kg Dex prior to OLT. ∗ P < 0.05, compared to Group S; # P < 0.05, compared to Group M; $ P < 0.05, compared to Group D2.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Dexmedetomidine Attenuates Orthotopic Liver Transplantation-Induced Acute Gut Injury via α 2 -Adrenergic Receptor-Dependent Suppression of Oxidative Stress

doi: 10.1155/2019/9426368

Figure Lengend Snippet: Blocking α 2A -AR siRNA counteracted the alleviation of oxidative stress by Dex in intestines of rats with OLT. The levels of oxidant ROS (a) and antioxidants including GST α 1 (b), SOD (c), and GSH (d) were measured in rat intestines. Data are represented as the mean ± standard deviation, n = 8 for each group. S: sham-operated group; M: the model group with OLT; D1: rats that were pretreated with 10 μ g/kg before OLT; D2: rats that were pretreated with 50 μ g/kg before OLT; B1: rats that received 500 g/kg atipamezole at 40 min before receiving 50 μ g/kg Dex prior to OLT; B2: rats that received 50 g/kg ARC239 at 40 min before receiving 50 μ g/kg Dex prior to OLT; B3: rats that received 1.5 mg/kg BRL-44408 at 40 min before receiving 50 μ g/kg Dex prior to OLT. ∗ P < 0.05, compared to Group S; # P < 0.05, compared to Group M; $ P < 0.05, compared to Group D2.

Article Snippet: The α 2A -AR siRNA duplexes (5′-CGAGCUGCAAGAUUAACGA-3′) targeting the rat α 2A -AR siRNA gene (gene ID: 25083; nucleotide accession number: NM_012739.3) were commercially obtained from Biomics (Jiangsu, China).

Techniques: Blocking Assay, Standard Deviation

Silencing of α 2A -AR siRNA reversed the protective role of Dex on cell apoptosis in IEC-6 cells with simulated H/R stimulation. (a) qRT-PCR data showing effective knockdown of α 2A -AR by siRNA transfection in IEC-6 cells. Control: untreated IEC-6 cells; NC-siRNA: IEC-6 cells transfected with nonspecific control siRNA; α 2A -AR siRNA: IEC-6 cells transfected with α 2A -AR-specific siRNA. (b) Results of the cell proliferation assay by Cell Counting Kit-8 in IEC-6 cells with different stimulations. (c) Summary of cell apoptosis data of IEC-6 cells with different stimulations. (d) Representative flow cytometry profiles showing the cell apoptosis assay by annexin V and propidium iodide staining, n = 6 for each group. A: control IEC-6 cells; B: IEC-6 cells with H/R treatment; C: IEC-6 cells that were pretreated with 1 nM Dex for 1 h before inducing H/R injury; D: IEC-6 cells with silencing of α 2A -AR siRNA; E: IEC-6 cells with silencing of α 2A -AR siRNA and H/R treatment; F: IEC-6 cells with silencing of α 2A -AR siRNA that were pretreated with Dex prior to H/R injury. ∗ P < 0.05, compared to Group A; # P < 0.05, compared to Group B; $ P < 0.05, compared to Group C.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Dexmedetomidine Attenuates Orthotopic Liver Transplantation-Induced Acute Gut Injury via α 2 -Adrenergic Receptor-Dependent Suppression of Oxidative Stress

doi: 10.1155/2019/9426368

Figure Lengend Snippet: Silencing of α 2A -AR siRNA reversed the protective role of Dex on cell apoptosis in IEC-6 cells with simulated H/R stimulation. (a) qRT-PCR data showing effective knockdown of α 2A -AR by siRNA transfection in IEC-6 cells. Control: untreated IEC-6 cells; NC-siRNA: IEC-6 cells transfected with nonspecific control siRNA; α 2A -AR siRNA: IEC-6 cells transfected with α 2A -AR-specific siRNA. (b) Results of the cell proliferation assay by Cell Counting Kit-8 in IEC-6 cells with different stimulations. (c) Summary of cell apoptosis data of IEC-6 cells with different stimulations. (d) Representative flow cytometry profiles showing the cell apoptosis assay by annexin V and propidium iodide staining, n = 6 for each group. A: control IEC-6 cells; B: IEC-6 cells with H/R treatment; C: IEC-6 cells that were pretreated with 1 nM Dex for 1 h before inducing H/R injury; D: IEC-6 cells with silencing of α 2A -AR siRNA; E: IEC-6 cells with silencing of α 2A -AR siRNA and H/R treatment; F: IEC-6 cells with silencing of α 2A -AR siRNA that were pretreated with Dex prior to H/R injury. ∗ P < 0.05, compared to Group A; # P < 0.05, compared to Group B; $ P < 0.05, compared to Group C.

Article Snippet: The α 2A -AR siRNA duplexes (5′-CGAGCUGCAAGAUUAACGA-3′) targeting the rat α 2A -AR siRNA gene (gene ID: 25083; nucleotide accession number: NM_012739.3) were commercially obtained from Biomics (Jiangsu, China).

Techniques: Quantitative RT-PCR, Knockdown, Transfection, Control, Proliferation Assay, Cell Counting, Flow Cytometry, Apoptosis Assay, Staining

Silencing of α 2A -AR siRNA erased the protective role of Dex on antioxidation in IEC-6 cells with simulated H/R stimulation. (a) Summary of ROS levels in IEC-6 cells with different treatments. (b) Representative fluorescence immunostaining images of Nrf2 in IEC-6 cells with different treatments. Scale bar, 100 μ m. (c–d) Expression of Nrf2, NQO1, and Keap1 proteins and mRNA levels in intestinal tissues. (e–g) Summary of the relative expression levels of the transcripts for the genes HMOX1 (e), SOD1 (f), and CAT (g) in IEC-6 cells with different treatments, n = 6 for each group. A: control IEC-6 cells; B: IEC-6 cells with H/R treatment; C: IEC-6 cells that were pretreated with 1 nM Dex for 1 h before inducing H/R injury; D: IEC-6 cells with silencing of α 2A -AR siRNA; E: IEC-6 cells with silencing of α 2A -AR siRNA and H/R treatment; F: IEC-6 cells with silencing of α 2A -AR siRNA that were pretreated with Dex prior to H/R injury. ∗ P < 0.05, compared to Group A; # P < 0.05, compared to Group B; $ P < 0.05, compared to Group C.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Dexmedetomidine Attenuates Orthotopic Liver Transplantation-Induced Acute Gut Injury via α 2 -Adrenergic Receptor-Dependent Suppression of Oxidative Stress

doi: 10.1155/2019/9426368

Figure Lengend Snippet: Silencing of α 2A -AR siRNA erased the protective role of Dex on antioxidation in IEC-6 cells with simulated H/R stimulation. (a) Summary of ROS levels in IEC-6 cells with different treatments. (b) Representative fluorescence immunostaining images of Nrf2 in IEC-6 cells with different treatments. Scale bar, 100 μ m. (c–d) Expression of Nrf2, NQO1, and Keap1 proteins and mRNA levels in intestinal tissues. (e–g) Summary of the relative expression levels of the transcripts for the genes HMOX1 (e), SOD1 (f), and CAT (g) in IEC-6 cells with different treatments, n = 6 for each group. A: control IEC-6 cells; B: IEC-6 cells with H/R treatment; C: IEC-6 cells that were pretreated with 1 nM Dex for 1 h before inducing H/R injury; D: IEC-6 cells with silencing of α 2A -AR siRNA; E: IEC-6 cells with silencing of α 2A -AR siRNA and H/R treatment; F: IEC-6 cells with silencing of α 2A -AR siRNA that were pretreated with Dex prior to H/R injury. ∗ P < 0.05, compared to Group A; # P < 0.05, compared to Group B; $ P < 0.05, compared to Group C.

Article Snippet: The α 2A -AR siRNA duplexes (5′-CGAGCUGCAAGAUUAACGA-3′) targeting the rat α 2A -AR siRNA gene (gene ID: 25083; nucleotide accession number: NM_012739.3) were commercially obtained from Biomics (Jiangsu, China).

Techniques: Fluorescence, Immunostaining, Expressing, Control