C1q/TNF-Related Protein 9 Protects Diabetic Rat Heart against Ischemia Reperfusion Injury: Role of Endoplasmic Reticulum Stress

Figure 1

CTRP9 protected diabetic heart against IR injury. Isolated hearts from HFD induced type 2 diabetic rats were subjected to control or IR protocol at the presence of different dosage of globular CTRP9 or equal amount of KH buffer. Cardiomyocytes apoptosis was determined by TUNEL staining and Caspase-3, Caspase-9, Caspase-12, and TNF-α ((c), (d), (e), and (f)) were examined by Western blot. GAPDH was used as loading control. Representative images (b) and bar graph (g) of apoptotic cardiomyocytes were shown. The apoptotic cells were detected by immunofluorescent staining with TUNEL ((b), upper panel), and DAPI staining was used to label the nuclei ((b), lower panel). Infarct size was determined by TTC staining ((i), upper panel) and was expressed as the percentage of infarct size/area at risk ((i), lower panel). LDH activity in the coronary effluent was measured and was expressed as milliunit/mL (h). The results were expressed as the mean ± SEM, per group. compared with control; compared with IR, compared with IR+0.3.

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