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Objective To investigate whether curcumin could inhibit cisplatin-induced apoptosis of HK-2 cells. Methods Using MTT methods to observe inhibitory effects of curcumin and cisplatin on the proliferation of HK-2 cell. Detecting caspases expression after curcumin and cisplatin treatment by Western blot. Results Cisplatin induced cell apoptosis, and the effect was dose-dependent(P＜0.05).Under the synergistic effect of curcumin and cisplatin on HK-2 cell, the number of apoptosis decreased(P＜0.05). In the same time the expression of Bcl-2 protein increased (P < 0.05) and the expression of Bcl-2 protein decreased (P < 0.05). Conclusions Cisplatin enhances the apoptosis of HK-2 cell in a dose-dependent manner, and is inhibited by curcumin. Curcumin can antagonize cisplatin-induced apoptosis in HK-2 by regulating the expressions of Bax and Bcl-2 protein.
RESUMO
<p><b>OBJECTIVE</b>To explore the effect of puerarin combined with felodipine on the mRNA and protein expression of apelin and APJ in renal tissue of renovascular hypertensive rat.</p><p><b>METHOD</b>Sixty-two Sprague-Dawley rats were used, of which 8 rats were randomly chosen as sham-operation group. The remaining rats were made for the rat model with renovascular hypertension. The renovascular hypertensive rats were randomly divided into 5 groups as follows: 4 groups which were treated with felodipine (0.8 mg x kg(-1) x d(-1)), puerarin (50 mg x kg(-1) x d(-1)), puerarin combined with felodipine (puerarin 25 mg x kg(-1) x d(-1) + felodipine 0.4 mg x kg(-1) x d(-1)) or captopril combined with felodipine (captopril 15 mg x kg(-1) x d(-1) x felodipine 0.4 mg x kg(-1) x d(-1)), and 1 group which was treated with distilled water. Drugs or distilled water were administered for 8 weeks. The expression of apelin and APJ mRNA and protein in ischemic and non-ischemic kidneys was assessed by RT-PCR or Western blot.</p><p><b>RESULT</b>Compared with sham-operation group, the expression of apelin mRNA and protein in ischemic and non-ischemic kidneys in model group was increased significantly (P < 0.01); the expression of APJ mRNA and protein in ischemic kidneys had no significance, while that in non-ischemic kidneys was decreased (P < 0. 01). Compared with model group, the expression of apelin mRNA and protein in ischemic and non-ischemic kidneys was decreased significantly in all drug-treated groups (P < 0.01); while that of APJ mRNA and protein in non-ischemic kidneys was upregulated (P < 0.01). Compared with felodipine group, the expression of apelin mRNA and protein in ischemic and non-ischemic kidneys was decreased (P < 0.01 or P < 0.05) in the group treated with both puerarin and felodipine; and the expression of APJ mRNA and protein in ischemic kidneys did not reach significant level, however, that was upregulated in non-ischemic kidneys (P < 0.01 or P < 0.05).</p><p><b>CONCLUSION</b>Puerarin downregulates the expression of apelin mRNA and protein in ischemic and non-ischemic kidneys, and upregulates that of APJ mRNA and protein in non-ischemic kidneys. Combination of puerarin and felodipine enhances the above-mentioned effects and shows no significant difference versus the combination of felodipine and captopril. The results suggest that puerarin regulates blood pressure and protects target organ through apelin/APJ pathway and that puerarin has synergetic effects with CCB.</p>