Article Text


Experimental research
Effects of fistular onion bulb extract on ischemia/reperfusion injury in cardiomyocytes of streptozotocin-induced diabetes mullitus rats
  1. Jun Zhou,
  2. Yanping Xu,
  3. Teng Wang
  1. Department Of Cardiology


Objective To investigate effects of fistular onion bulb extract (FOB) preventing ischemia/reperfusion (I/R) injury in cardiomyocytes of streptozotocin-induced diabetes mellitus rats.

Methods Diabetes rats by streptozotocin-induced were fed FOB (100 g/kg/day) from six to 14 week of age. Hearts models of I/R which randomly divided into control group, diabetes group, FOB control and diabetes groups were observed changes of heart function through using Langendorff-perfusion system. Fluorescence intensity of intracellular Ca2+ was detected with Flup-3/AM loading by laser scanning confocal microscope. ICa-L was recorded via whole-cell patch clamp technique in enzymatically dissociated single cardiomyocytes.

Results In diabetes group, values of LVDP, LVEDP, (dp/dtmax) and CF were all significantly decreased, and dp/dtmin were increased (compared with normal control group, p<0.01, respectively). But every parameter mentioned above such as LVDP, LVEDP, dp/dtmax, CF was increased, and dp/dtmin was obviously decreased in FOB diabetes group (compared with diabetes group, p<0.01, respectively). Fluorescence intensities of intracellular free Ca2+ were markedly stronger after influence of I/R injury (compared with normal control group, p<0.01). Current density of ICa-L was significantly decreased, and I–V curve was changed up to the top, as soon as the peak clamp potential was −30 mV with same I/R condition in diabetes rats. In FOB diabetes group, fluorescence intensities of intracellular free Ca2+ were significantly reduced in I/R injury procedure (compared with diabetes group, p<0.01). ICa-L was partly recovered near normal control group, and I–V curve was changed among normal control and diabetes group. When clamp voltage was −20 mV, the current densities of ICa-L were significantly decreased from (−8.17±2.07) pA/pF in normal control group to (−3.21±0.54)pA/pF in diabetes group (p<0.01). (−7.14±2.17) pA/pF in FOB control group (compared with normal control, p>0.05, and (−6.81±0.76) pA/pF in FOB diabetes (compared with normal group, p<0.05, and with diabetes group, p<0.01, and with FOB control group, p>0.05).

Conclusion Poor heart function was tightly correlate to that (Ca2+)i was increased and ICa-L was decreased with I/R injury in diabetes rat hearts. FOB- treated could significantly inhibit I/R injury induced severely cardiac performance, which was attributed to that FOB might adjust ICa-L influx, and normalise balance of intercellular (Ca2+)i, as soon as blocked Ca2+ overload trigged by effects of Ca2+-induced Ca2+ release in diabetes cardiomyocytes.

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