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Effects of RIpreC on the expression of Bcl-2 ( A , B , F , G ), Bax ( A , C , F , H <t>),</t> <t>caspase-3</t> ( A , D , F , J ), and TUNEL-positive neurons ( A , E ) in the ischemic brain. Bcl-2 immunoreactivity in the perilesional cortex and its protein level were significantly increased in the RIpreC group compared the IR group. By contrast, Bax immunoreactivity and its protein level were significantly reduced in the RIpreC group compared with the IR group. The Bax/Bcl-2 ratios were also significantly reduced in the RIpreC group compared with the IR group ( I ). Subsequently, the number of TUNEL-positive neurons (arrow) and the ratios of caspase-3 positive to NeuN-positive neuron in the perilesional cortex were significantly decreased in the RIpreC group compared with the IR group ( E , K , L ). Mean ± standard error. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. Scale bar = 50 μm ( A ) and 25 μm ( K ). ( n = 4–11 in each group)
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Effects of RIpreC on the expression of Bcl-2 ( A , B , F , G ), Bax ( A , C , F , H <t>),</t> <t>caspase-3</t> ( A , D , F , J ), and TUNEL-positive neurons ( A , E ) in the ischemic brain. Bcl-2 immunoreactivity in the perilesional cortex and its protein level were significantly increased in the RIpreC group compared the IR group. By contrast, Bax immunoreactivity and its protein level were significantly reduced in the RIpreC group compared with the IR group. The Bax/Bcl-2 ratios were also significantly reduced in the RIpreC group compared with the IR group ( I ). Subsequently, the number of TUNEL-positive neurons (arrow) and the ratios of caspase-3 positive to NeuN-positive neuron in the perilesional cortex were significantly decreased in the RIpreC group compared with the IR group ( E , K , L ). Mean ± standard error. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. Scale bar = 50 μm ( A ) and 25 μm ( K ). ( n = 4–11 in each group)
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Effects of RIpreC on the expression of Bcl-2 ( A , B , F , G ), Bax ( A , C , F , H <t>),</t> <t>caspase-3</t> ( A , D , F , J ), and TUNEL-positive neurons ( A , E ) in the ischemic brain. Bcl-2 immunoreactivity in the perilesional cortex and its protein level were significantly increased in the RIpreC group compared the IR group. By contrast, Bax immunoreactivity and its protein level were significantly reduced in the RIpreC group compared with the IR group. The Bax/Bcl-2 ratios were also significantly reduced in the RIpreC group compared with the IR group ( I ). Subsequently, the number of TUNEL-positive neurons (arrow) and the ratios of caspase-3 positive to NeuN-positive neuron in the perilesional cortex were significantly decreased in the RIpreC group compared with the IR group ( E , K , L ). Mean ± standard error. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. Scale bar = 50 μm ( A ) and 25 μm ( K ). ( n = 4–11 in each group)
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Effects of RIpreC on the expression of Bcl-2 ( A , B , F , G ), Bax ( A , C , F , H <t>),</t> <t>caspase-3</t> ( A , D , F , J ), and TUNEL-positive neurons ( A , E ) in the ischemic brain. Bcl-2 immunoreactivity in the perilesional cortex and its protein level were significantly increased in the RIpreC group compared the IR group. By contrast, Bax immunoreactivity and its protein level were significantly reduced in the RIpreC group compared with the IR group. The Bax/Bcl-2 ratios were also significantly reduced in the RIpreC group compared with the IR group ( I ). Subsequently, the number of TUNEL-positive neurons (arrow) and the ratios of caspase-3 positive to NeuN-positive neuron in the perilesional cortex were significantly decreased in the RIpreC group compared with the IR group ( E , K , L ). Mean ± standard error. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. Scale bar = 50 μm ( A ) and 25 μm ( K ). ( n = 4–11 in each group)
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Image Search Results


Effects of RIpreC on the expression of Bcl-2 ( A , B , F , G ), Bax ( A , C , F , H ), caspase-3 ( A , D , F , J ), and TUNEL-positive neurons ( A , E ) in the ischemic brain. Bcl-2 immunoreactivity in the perilesional cortex and its protein level were significantly increased in the RIpreC group compared the IR group. By contrast, Bax immunoreactivity and its protein level were significantly reduced in the RIpreC group compared with the IR group. The Bax/Bcl-2 ratios were also significantly reduced in the RIpreC group compared with the IR group ( I ). Subsequently, the number of TUNEL-positive neurons (arrow) and the ratios of caspase-3 positive to NeuN-positive neuron in the perilesional cortex were significantly decreased in the RIpreC group compared with the IR group ( E , K , L ). Mean ± standard error. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. Scale bar = 50 μm ( A ) and 25 μm ( K ). ( n = 4–11 in each group)

Journal: Translational Stroke Research

Article Title: Remote Ischemic Preconditioning Exerts Neuroprotective Effects Via the PGC-1α/FNDC5/BDNF Pathway in Focal Brain Ischemia of Rats

doi: 10.1007/s12975-026-01422-z

Figure Lengend Snippet: Effects of RIpreC on the expression of Bcl-2 ( A , B , F , G ), Bax ( A , C , F , H ), caspase-3 ( A , D , F , J ), and TUNEL-positive neurons ( A , E ) in the ischemic brain. Bcl-2 immunoreactivity in the perilesional cortex and its protein level were significantly increased in the RIpreC group compared the IR group. By contrast, Bax immunoreactivity and its protein level were significantly reduced in the RIpreC group compared with the IR group. The Bax/Bcl-2 ratios were also significantly reduced in the RIpreC group compared with the IR group ( I ). Subsequently, the number of TUNEL-positive neurons (arrow) and the ratios of caspase-3 positive to NeuN-positive neuron in the perilesional cortex were significantly decreased in the RIpreC group compared with the IR group ( E , K , L ). Mean ± standard error. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. Scale bar = 50 μm ( A ) and 25 μm ( K ). ( n = 4–11 in each group)

Article Snippet: # p < 0.05 (Mann–Whitney U test), # p < 0.01 (Student’s t-test), Scale bar = 1 mm ( B ). ( n = 5–11 in each group) Co-localization of mouse anti-neuronal nuclei (NeuN) antibody (1:200; a marker of neurons; ab104224; Abcam plc, Cambridge, UK) with rabbit anti-caspase-3 antibody (1:200; 19677-1-AP; Proteintech, USA) immunoreactivities was examined using immunofluorescence staining.

Techniques: Expressing, TUNEL Assay

Effects of PGC-1αInhibition by SR-18,292. Inhibition of PGC-1α blunted the neuroprotective and neurorestorative effects of RIpreC ( A – F ). No changes in brain infarctions, neurological scores, and sensorimotor functions were observed in the RIpreC-treated SR-18,292 group compared with the IR group. Immunohistochemical analysis of the rectangular areas in A showed that immunoreactivities of PGC-1α, FNDC5, BDNF, and caspase-3 surrounding the lesion in the RIpreC-treated SR-18,292 group were similar to those in the IR group ( G – K ). Scale bar = 50 μm ( G ). ( n = 5–11 in each group)

Journal: Translational Stroke Research

Article Title: Remote Ischemic Preconditioning Exerts Neuroprotective Effects Via the PGC-1α/FNDC5/BDNF Pathway in Focal Brain Ischemia of Rats

doi: 10.1007/s12975-026-01422-z

Figure Lengend Snippet: Effects of PGC-1αInhibition by SR-18,292. Inhibition of PGC-1α blunted the neuroprotective and neurorestorative effects of RIpreC ( A – F ). No changes in brain infarctions, neurological scores, and sensorimotor functions were observed in the RIpreC-treated SR-18,292 group compared with the IR group. Immunohistochemical analysis of the rectangular areas in A showed that immunoreactivities of PGC-1α, FNDC5, BDNF, and caspase-3 surrounding the lesion in the RIpreC-treated SR-18,292 group were similar to those in the IR group ( G – K ). Scale bar = 50 μm ( G ). ( n = 5–11 in each group)

Article Snippet: # p < 0.05 (Mann–Whitney U test), # p < 0.01 (Student’s t-test), Scale bar = 1 mm ( B ). ( n = 5–11 in each group) Co-localization of mouse anti-neuronal nuclei (NeuN) antibody (1:200; a marker of neurons; ab104224; Abcam plc, Cambridge, UK) with rabbit anti-caspase-3 antibody (1:200; 19677-1-AP; Proteintech, USA) immunoreactivities was examined using immunofluorescence staining.

Techniques: Inhibition, Immunohistochemical staining