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Fig. 3 | Molecular Brain

Fig. 3

From: Acute upregulation of neuronal mitochondrial type-1 cannabinoid receptor and it’s role in metabolic defects and neuronal apoptosis after TBI

Fig. 3

MtCB1 regulated neuronal apoptosis following injury. Both in vivo and vitro of wild type 24 h post injury, TUNEL study showed THC and HU210 protected neurons from apoptosis while AM251 promoted apoptosis compared with vehicle (a, b). THC, HU-210 or AM251 did not affect cellular apoptosis both in vivo and vitro of CB1−/− (c, d). Compared with vehicle, hemopressin or HU210-biotin did not affect cellular apoptosis in vitro of wild type but reversely mediated apoptosis in vivo of wild type (e, f). Western blot analysis showed HU210 or AM251 reversely mediated mitochondrial cyt c and AIF release of wild type both in vivo and vitro but not in CB1−/− mice (g, h). Nuclear morphology was indicated by DAPI staining and DNA breaks were detected by TUNEL analyses. Tom20 is a mitochondrial protein. bar: 25 μm. Data were expressed as mean ± SE (#p < 0.05 versus vehicle, ##p < 0.01 versus vehicle, ###p < 0.001 versus vehicle)

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