Skin wound healing is a process that involves the cooperation of different cells (including fibroblasts, monocytes, macrophages, endothelial cells, and epidermal cells), growth factors, and cytokines [15]. After injury, healing and repair of skin damage in diabetic patients shows a significant decrease. Many evidences show that high concentrations of glucose have destructive effects on the function of different cells in different tissues and organs [10]. Our results showed that the healing process leading to wound closure is faster in the hyperglycemic groups treated with the extract compared to the control group. Meanwhile, in the group of hyperglycemia without treatment, the mentioned events are delayed. The results of this study are consistent with the results of other studies which showed that high glucose disrupts the migration and proliferation of cells and causes damage to skin fibroblasts [10, 16]. A study showed that the hydroalcoholic extract of Prosopis farcta leaves is effective in reducing blood glucose [9]. In a research, it was shown that Quercetin, which is a type of flavonoid, inhibits the expression of inflammatory cytokines. Therefore, it seems that due to the presence of flavonoids in the P. farcta, which is probably related to anti-inflammatory effects through the inhibition of inflammatory mediators, a reduction in the period of inflammation and acceleration of the healing of diabetic wounds have been observed [15]. The results of the study showed that flavonoids and triterpenoids increase wound contraction and epithelization [15]. The use of medicinal plants is especially significant when common treatments are not able to control the disease, and the patient needs insulin administration [6].

MTT results indicated that the best concentration of the extract for this study was 200 μg/ml (optimal concentration) and the plant extract increased cell survival, growth and proliferation. Concentrations higher or lower than these cause little damage to the cell.

The SEM results showed that the PLA scaffold in the in vitro environment is suitable for 3D cell culture and the cells grow well on this scaffold. The production of three-dimensional polylactic acid scaffolds made by wet electrospinning method has a porosity of over 80% and low density [13]. The results of a research showed that the PLA/CS (polylactic acid/chitosan) scaffold prepared by electrospinning method is a scaffold with biocompatibility and surface topography suitable for adhesion, survival and cell culture and does not cause any negative side effects due to grafting. This scaffold along with the simultaneous cultivation of fibroblasts and its placement in the wound improves the wound healing process. It seems that this scaffold has caused an increase in the number of fibroblasts at the wound site and an increase in the amount of collagen and possibly also an increase in the amount of angiogenesis, thus accelerating and shortening the healing time of the wound [17].

The results of our study showed that the expression level of HO1 and SOD1 genes in hADMSC in hyperglycemic environment (50, 25 and 75 mM) under treatment with plant extract (200 μg/ml) decreased compared to the control group but in the hyperglycemic group, the expressions increased with the mentioned concentrations and without extract treatment. These genes have an antioxidant and cell protective effect. When the cell is cultured in high glucose environment, due to the destructive effect of glucose, cell growth decreases, but by adding the extract, the antioxidant effect increases which causes the conditions to approach the normal condition and the expression of the mentioned genes decreases. Prosopis farcta with the antioxidant compounds such as apigenin and vicenin-2 [18] is effective in the treatment of diabetes and its complications. Increased levels of HO1 result in increased levels of the antioxidant, bilirubin and anti-apoptotic, carbon monoxide, which are responsible for neutralizing free radicals, ICAM-1, VCAM-1, TNF and IL-18 [18]. Our study showed the antioxidant genes HO1 and SOD1 increase significantly in the condition that the cell is in a hyperglycemic environment to trap the ROS produced in the cell.

In eukaryotic cells, mitochondria are double-membrane organelles that provide the main energy for intracellular events through aerobic respiration and oxidation. During this process, the concentration of protons and other ions is asymmetrically distributed on both sides of the inner membrane, and the mitochondria show a negative potential difference, that is, the mitochondrial membrane potential (MMP) [19,20,21]. As a measure of mitochondrial function, MMP can indicate the healthy state of cells [22, 23]. Normal MMP usually fluctuates from − 150 to − 180 mV and can maintain stable biological activities, including ATP synthesis [24], signal transduction, ion exchange [25]. However, any abnormality in the level of MMP, even a small change, will have a great impact on mitochondrial function, which causes mitochondrial dysfunction [26]. For example, loss of MMP level is a signal of some cellular disorder events that lead to autophagy, apoptosis and necrosis [27]. Recent reports showed that many diseases, such as diabetes, are associated with the loss of MMP [28].

In a study conducted on the relationship between mitochondrial membrane potential and sperm quality and fertility, it was shown that high mitochondrial membrane potential indicates normal and more mobile sperm. Considering that sperm mitochondrial membrane contains cytochrome C, in case of destruction of mitochondrial membrane by ROS, this cytochrome is released from mitochondria and activates caspases and induces apoptosis phenomenon. Apoptosis can aggravate DNA damage caused by ROS [29]. Oxidative stress causes damage to the nuclear and mitochondrial DNA in sperm cells and a decrease in glutathione and an increase in markers of oxidative stress and lipid peroxidation in the testicles of diabetics, all of which occur as a result of chronic hyperglycemia and an increase in free radicals that cause the inactivation of antioxidant factors [30]. In the present study, the increase in glucose concentration caused a decrease in mitochondrial membrane potential and apoptosis.

Induction of type II diabetes in mice caused a significant decrease in BCL2 protein expression, an increase in Bax protein expression, and as a result, an increase in the ratio of Bax/Bcl-2 and a significant increase in apoptosis [31]. Increased oxidative stress and defects in mitochondrial function play a pivotal role in inducing apoptotic cell death. The opening of the mitochondrial permeability transition pore causes the depolarization of the transmembrane potential, the release of calcium (Ca2+) and cytochrome C, and the loss of oxidative phosphorylation, which leads to the loss of cell viability [32].

It has been shown that high concentration of glucose can cause the death of PC12 cells (similar to fetal neurons) through the internal pathway of apoptosis with the activation of caspases 9 and 3 [33]. DNA fragmentation is a biochemical hallmark of apoptosis. The enzyme responsible for DNA fragmentation/apoptosis is caspase-activated DNase.

Therefore, according to the results of our study, the harmful effects caused by glucose induce a decrease in the mitochondrial membrane potential. However, by treating the cells with hydroalcoholic extract of Prosopis farcta, we saw a decrease in DNA fragmentation and an increase in mitochondrial membrane potential.