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. 2022 Apr 4;12(7):3196–3216. doi: 10.7150/thno.71029

Figure 8.

Figure 8

Knockdown of neuronal PTRF does not enhance PLA2G4A inhibition induced neuroprotection after cerebral I/R injury. (A) Western blot analyses of the expression levels of the Caspase3, Bax, and Bcl-2 in AAV-shRNA transfected primary neuronal cells co-treated with AACOCF3 (0.010 mM) under OGD/R. (B) The experimental protocol used in AAV-shRNA transfected mice co-treated with AACOCF3 (25 mg/kg body weight) after I/R injury. (C) The corner turn test was analyzed using the laterality index in AAV-shRNA transfected mice co-treated with AACOCF3 (25 mg/kg body weight) after I/R injury (n = 6). (D) Neurological deficit was assessed throughout recovery in the mice at 24 h and 72 h post-cerebral I/R injury (n = 7). (E-F) TTC stained brain slices showing infarct volume (white), and the infarct volume was measured in AAV-shRNA transfected mice co-treated with AACOCF3 (25 mg/kg body weight) after I/R injury (n = 3). (G) Mouse survival rates at 3 d post-cerebral I/R injury in the mice (n = 25). (H) The expression levels of Caspase3, Bax, and Bcl-2 in the ipsilateral penumbras of the mice after cerebral I/R injury.