Protective effects ofZygophyllum albumextract against deltamethrin-induced hyperglycemia and hepato-pancreatic disorders in rats

Abstract

The current study was designed to investigate the possible mechanism involved in hyperglycemia induced by chronic exposure to deltamethrin (DLM) in rat and to assess whether this damage is amenable to modulation by Zygophyllum album. DLM, a synthetic pyrethroid pesticide, was administrated at a dose of 4 mg/kg body mass, during 60 days. Compared with control, DLM showed a significant increase of blood glucose (p ≤ 0.01) and glycosylated hemoglobin levels (p ≤ 0.01) and a clear decrease (p ≤ 0.01) of insulin and total hemoglobin levels. In addition, hepatic glycogen content and the activity of hexokinase decreased (p ≤ 0.01), whereas the activities of glucose-6-phosphatase and glycogen phosphorylase were significantly increased (p ≤ 0.01). Moreover, pancreatic lipid peroxidation (TBARS level) was higher (p ≤ 0.01) and oxidative stress biomarkers (SOD, CAT, GPx, and GSH) were altered owing to DLM toxicity. However, Z. album, when combined with DLM, significantly ameliorated almost all the hepato-pancreatic disorders induced by DLM alone. Furthermore, Z. album supplement was found to be effective in preserving the normal histological appearance of hepatic and pancreatic tissue. In conclusion, this study suggested that, owing to its antioxidant effects, methanolic extract of Z. album (MEZAL) can potentially prevent the hyperglycemia observed in DLM-treated group.

Zygophyllum albumaqueous extract reduces glycemia and ameliorates lipid profile and oxidative damage in hypercholesterolemic-diabetic rats

“…Our study has demonstrated a significant decrease in TBARS levels and an improved antioxidant enzymes activity (SOD, GSH-PX, GSSH-Red and CAT) in all tissue after Z. album extract supplementation. These finding are similar with those of Feriani et al (2016), who note a significant lowered lipid peroxidation in the pancreas in deltamethrin-induced hyperglycemic rats and an ameliorated levels of SOD, CAT and GSH-Px with Z. album extract treatment. The protective effect of Z. album extract could be explained by its ability to reduce the level of oxidative stress by the inhibition of ROS generation; Z. album extract can help to protect the β -cells structure and function in DM rats via a reduction of ROS production and the improvement of antioxidant enzymes.…”

“…However, Z. album extract exhibited a notable decrease in HbA 1 C of DM rats, which reflects the beneficial action of this extract in control of diabetes complications. Moreover, Feriani et al (2016) showed that administration of methanoic extract Z. album leaves for 60 days prevented a significant elevation in HbA 1 C, thereby increasing the level of hemoglobin in deltamethrin-induced-hyperglycemic treated rats. This could be due to the restoration of blood glucose level, consequently reducing the level of hemoglobin glycosylation during the experimental period.…”

“…These results are in agreement with those of other authors; ethanol Cnidoscolus aconitifolius leaves extracts significantly increased the insulin levels of DM rats (Achi et al , 2017); also, hydroalcoholic extract of aerial parts of Schroederichthys chilensis may be effective in maintaining glucose homeostasis by release of insulin as well as via increasing insulinotropic activity (Schneider et al , 2015). Feriani et al (2016), had demonstrated that levels of both plasma glucose and insulin were significantly reversed after methanoic extract of Z. album leaves treatment in deltamethrin-induced hyperglycemic rats. The antihyperglycemic potential of methanoic extract of Z. album could be due to the increased release of insulin from the existing β -cells population of the islets of Langerhans and enhanced utilization of glucose by peripheral tissues.…”

Zygophyllum album aqueous extract reduces oxidative damage in erythrocytes and attenuates pro-inflammatory markers in hypercholesterolemic-diabetic rats

“…En effet, une synthèse accrue du TNF-α et de l'IL-6 est observée, ce qui pourrait être due à l'augmentation du stress oxydatif par l'intermédiaire des cellules immunitaires activées [46]. Il est bien établi que le cholestérol provoque une inflammation et les métabolites oxydés du cholestérol peuvent prendre part à la stimulation de l'expression des marqueurs de l'inflammation [47]. De plus, l'homocystéine agit contre l'inflammation induite -par le cholestérol in vivo chez le rat.…”

“…De plus, l'homocystéine agit contre l'inflammation induite -par le cholestérol in vivo chez le rat. Cet effet pourrait être médié par un processus lié à l'activateur du plasminogène tissulaire [47]. Par ailleurs, les travaux de Feriani et al, [48] ont également montré que, chez le rat, l'induction du diabète expérimental par la deltaméthrine, entraine une inflammation avec des teneurs élevées en CRP et TNF-α.…”