Diabetic nephropathy is a grievous public health problem, which considered to among the grievous life-threatening complications of diabetes mellitus, and among the most important cause of end-stage renal disease (ESRD) [12]. Diabetic nephropathy occurs in morbidity reach up to 30 ~ 40% of diabetes complications. Diabetic nephropathy is featured by augmented proteinuria and glomerular filtration dysfunction in the clinical. There are some significant pathological changes in the shape and function of the renal, for example, renal microvasculature disruption, glomerular capillaries, tubular interstitial damage renal hypertrophy and expansion of the extracellular matrix [13]. Diabetic nephropathy brings great economic burden to people, and the prognosis of patients is poor, and the morbidity and mortality are high, which has caused widespread concern and research. Although treatments for diabetic nephropathy continue to develop, morbidity and mortality appear also to be increasing [14]. Therefore, seeking for more efficacious selectable treatment from officinal herbs in reducing the incidence and/or mortality of diabetic nephropathy is ongoing.
Raspberry Ketone is a well-known traditional Chinese medicine. In recent years, it has become a research hotspot because of its various biological activities such as anti-hyperglycemic, antioxidant, anti-inflammatory and neuroprotective [9–11]. The plants are rich in ketone compounds and are a good anti-diabetic drug, which can further explore the effect of the plant extracts on diabetic complications such as renal disease. The current research, consequently, appraised the protective effect of Chinese herbal extracts for DN in STZ-induced diabetic mice.
Oxidative stress plays an important role that has been incriminated in the nosogenesis of DN [15]. Excessive blood glucose is given rise to overproduction of oxidative stress, which has been intimately related to the occurrence and progress of DN [16–20]. Raising blood glucose is given rise to the overproduction of oxidative stress in the renal, which is given rise to the apoptosis of proximal tubular epithelial cells and mechanical cells and the depletion of phagocytes, which is the progression of diabetic nephropathy A phase is set [24, 25]. Raising biological activities of antioxidant enzymes alleviate oxidative stress, and foregoing research studies have shown that some antioxidant enzymes are decreased and lipid peroxidations are raised in DN [18]. Previous research has discovered that malondialdehyde with lipid peroxidation production was markedly raised, while the biological activity of SOD, GSH-PX and CAT was in diabetic nephropathy animals with a downturn [17, 26]. The research discovered that after treatment with raspberry ketone, diabetic mice markedly raised the biological activities of the internal SOD, GSH-PX and CAT, and concurrently given rise to a descendant in the malondialdehyde of lipid peroxidation production level. It validates that raspberry ketone has a beneficial antioxidant effect, while the mechanisms needed further investigation.
The excessive secretion of the pro-inflammatory cytokine has been put forward to bring into play an essential function on the occurrence and progression of DN [21–23]. Preceding experimental research has found that the production level of pro-inflammatory cytokines, for example, IL-1β and IL-6, TNF-α is increased in diabetic nephropathy [27, 28]. Stimulating an increase in the expression of various pro-inflammatory cytokines goes through the stimulation of NF-κB pathway when the organism produces oxidative stress, thus damaging the renal tissue [29]. Foregone experimental studies have shown that pro-inflammatory cytokines affected renal function and renal damage in a few mechanistic pathways [20, 30, 34]. Furthermore, the excessive release of pro-inflammatory cytokines in DN may give rise to the infiltration of macrophages, which successively injures the glomerular and causes excessive the level of urine micro-albumin [27, 31, 32]. Our experimental results showed that the production of TNF-α, IL-6 and IL-1β increased in diabetic nephropathy model control mice, which were markedly declined by raspberry ketone treatment. These results indicated that raspberry ketone may improve the renal function by reducing the expression of several pro-inflammatory cytokines, while the mechanisms needed further investigation.
The abnormal excretion of creatinine and urine micro-albumin is regarded as an important clinical pathological sign of diabetic nephropathy [35, 36]. Injuries to the renal in STZ-induced diabetic nephropathy animals are obvious with the increase in serum creatinine and the decrease in urine creatinine, which are suggestive of the abatement in creatinine clearance. Our experiments discover that raspberry ketone therapy reduced serum creatinine and raised urine creatinine levels in diabetic mice, indicating an enhancement in the renal functions of diabetic animals of the raspberry ketone therapy.
In our experimental animal model with revulsive diabetic nephropathy, animal ultrasound analysis of diabetic mice indicated noteworthy that the renal lesion was serious in diabetic nephropathy model group but the kidneys of the treated mice were similar in size to normal mice and the loss of integrity of basement membrane and was improved. Renal interstitial edema also was improved. We prove that raspberry ketone improved a few representative changes in diabetic nephropathy, namely, renal inflammation, renal hypertrophy, loss of integrity of renal basement membrane and renal interstitial edema, while the specific pathological analysis needed further investigation.