Objective: Wound temperature is one of the wound biomarkers representing the wound healing progress. The diabetic wound is associated with a prolonged inflammation phase marked by an increasing wound temperature and erythematous wound. Purple sweet potato extract (PSP), an anthocyanin-rich plant, improved wound healing in both diabetic and non-diabetic wounds in animal studies. This study aims to know the effect of purple sweet potato ethanol extract on wound temperature and erythema in streptozotocin-induced diabetic rats.
Methods: Rats were divided into four groups: normal rats + gel placebo; diabetic rats + gel placebo; diabetic rats + PSP 10%; and diabetic rats + PSP 15%. Diabetes mellitus was induced by streptozotocin injection. After diabetic confirmation, the back of the rats was excised and the gel was administered daily for 14 days. The wound temperature was measured at the wound surface using infrared thermography on days 0, 3, 7, and 14. The wounds were photographed and erythema analysis was conducted using Corel Photo paint®.
Results: Diabetic wounds exhibited higher surface temperature compared with the normal wound (37.08°C ± 0.29 vs 35.13°C ± 0.46) on day 14 of examination and topical application the purple sweet potato ethanol extract gel 10% and 15% markedly decreased the wound temperature at day 7 and 14 compared with the diabetes wound (p<0.0001). Wound erythema was significantly reduced in the PSP 10% and 15% diabetic wound treatment groups on day 14 (p<0.05).
Conclusion: Purple sweet potato extract gel treatment was found to have the potential to reduce inflammation in diabetic wounds.
Tag Archives: diabetes
The Assessment of Reperfusion Inflammatory Injury in Ischemic Preconditioned Diabetic Rats
Objective: The assessment of systemic reperfusion injury and the contractile force of the peripheral muscles post-acute ischemia of the hind limbs in healthy versus diabetic ischemic preconditioned rats. Method: The study included 16 Wistar rats divided into two groups: the control group and the diabetic ischemic preconditioned group. Acute ischemia was induced, followed by reperfusion. The assessment of reperfusion injury used biochemical, histopathological and functional determinations (peak tetanic tension-PTT, specific tension-ST). Results: Ischemia-reperfusion injury was more severe in control group regarding creatine-kinase (CK) (CK1=470.13 IU/L versus CK2=230.88 IU/L, p=0.0001) and myoglobin (390.25 ng/mL versus 47.99 ng/mL, p=0.025). Cytolysis enzymes were significantly increased in diabetic preconditioned rats (Alanine aminotransferase ALAT1=46 IU/L, ALAT2=167.8 IU/L, p=0.02; Aspartate aminotransferase ASAT1=106 IU/L, ASAT2=237.5 IU/L, p=0.016). Functional assessment (PTT and ST) highlighted roughly equal values. A paradoxical response occurred in diabetic rats (the contractile force increased during the period of the stimulation). Histopathological findings showed that rhabdomyolysis was more severe in the control group, while inflammatory systemic response due to reperfusion injury was less expressed in diabetic ischemic preconditioned rats. Conclusions: Ischemic preconditioning reduces the severity of reperfusion injury and allows the preservation of contractile muscle function in diabetic rats.