Ameliorative effects of Coccinia grandis leaf extract on Diabetes-Induced alterations of glucose metabolism, Cox activity and histological changes in Brain of Wistar Rats

2021 ◽  
Vol 12 (3) ◽  
pp. 1967-1976
Author(s):  
Bhaskar Nagilla ◽  
Bharathi Appidi ◽  
Pratap Reddy K

Coccinia grandis has been used in tribal populations of India both as food and medicine, but it has been not reported to be a neuroprotective agent yet. The present study was designed to evaluate the protective effects of Coccinia grandis leaf extract on diabetes induced brain damage of Wistar rats. This study reports the protective effect of methanolic leaf extract of Coccinia grandis against STZ induced diabetes in rats. Metformin (150mg/kg body wt.) was used as a reference drug. The enzymes of the polyol pathway and its related substrates were studied in the brain tissue. The effect of Coccinia on Cyclooxygenase (COX) and Prostaglandin peroxidise (PG) was also studied. Diabetes induced rats showed a significantly increased activity of Aldose reductase, Sorbitol dehydrogenase, Glucose-6-phosphodehydrogenase, whereas the decreased activity of Hexokinase. The content of Glucose, Sorbitol significantly increased in rat brain. Sodium potassium ATPase activity was also decreased in diabetic rats. COX, PG peroxidase was increased. Histological alternations were induced in the hippocampus of STZ treated diabetic rats. Oral administration of Coccinia leaf extract (200mg/kg) of body weight to diabetic rats for 21 days efficiently attenuated the parameters studied. A decreased activity of brain AR, sorbitol dehydrogenase, glucose-6-dehydrogenase was observed along with the increase in Hexokinase and Sodium potassium ATPase activity. It also showed decreased content of glucose and Sorbitol. Diabetes induced brain damage in the hippocampus and cerebral cortex was restored with Coccinia treatment. Decreased COX and PG peroxidase suggest its protection against inflammation. The current results suggest that Coccinia grandis leaf extract exerts the potential ability to reverse the progression of hyperglycemia and its concomitant induced brain damage.

2020 ◽  
Vol 17 (4) ◽  
pp. 510-517
Author(s):  
Santiago Ortega-Gutierrez ◽  
Brandy Jones ◽  
Alan Mendez-Ruiz ◽  
Pankhil Shah ◽  
Michel T. Torbey

Background: Hypoxic-ischemic encephalopathy (HIE) is a major cause of pediatric and adult mortality and morbidity. Unfortunately, to date, no effective treatment has been identified. In the striatum, neuronal injury is analogous to the cellular mechanism of necrosis observed during NMethyl- D-Aspartate (NMDA) excitotoxicity. Adenosine acts as a neuromodulator in the central nervous system, the role of which relies mostly on controlling excitatory glutamatergic synapses. Objective: To examine the effect of pretreatment of SCH58261, an adenosine 2A (A2A) receptor antagonist and modulator of NMDA receptor function, following hypoxic-ischemia (HI) on sodium- potassium ATPase (Na+, K+-ATPase) activity and oxidative stress. Methods: Piglets (4-7 days old) were subjected to 30 min hypoxia and 7 min of airway occlusion producing asphyxic cardiac arrest. Groups were divided into four categories: HI samples were divided into HI-vehicle group (n = 5) and HI-A2A group (n = 5). Sham controls were divided into Sham vehicle (n = 5) and Sham A2A (n = 5) groups. Vehicle groups were pretreated with 0.9% saline, whereas A2A animals were pretreated with SCH58261 10 min prior to intervention. Striatum samples were collected 3 h post-arrest. Sodium-potassium ATPase (Na+, K+-ATPase) activity, malondialdehyde (MDA) + 4-hydroxyalkenals (4-HDA) and glutathione (GSH) levels were compared. Results: Pretreatment with SCH58261 significantly attenuated the decrease in Na+, K+-ATPase, decreased MDA+4-HDA levels and increased GSH in the HI-A2A group when compared to HIvehicle. Conclusion: A2A receptor activation may contribute to neuronal injury in newborn striatum after HI in association with decreased Na+, K+-ATPase activity and increased oxidative stress.


1985 ◽  
Vol 5 (3) ◽  
pp. 177-181 ◽  
Author(s):  
Ronald J. Hené ◽  
Peter Boer ◽  
Hein A. Koomans ◽  
Evert J. Dorhout Mees

2018 ◽  
Vol 29 (4) ◽  
pp. 411-416 ◽  
Author(s):  
Aminat Omolola Imam-Fulani ◽  
Kamaldeen Olalekan Sanusi ◽  
Bamidele Victor Owoyele

Abstract Background This study was carried out to investigate the effects of acetone extract of Cola nitida on brain Na+/K+-ATPase activity and spatial memory of healthy and streptozotocin (STZ)-induced diabetic female Wistar rats. Methods Forty-two female Wistar rats were used for this study and were randomly distributed into six groups (n=7). Rats in group 1 were used as control and were administered normal saline; group 2 rats were healthy rats administered 50 mg/kg of kola nut extract per day; group 3 rats were healthy rats administered 100 mg/kg of kola nut extract per day; group 4 rats were a diabetic group also administered normal saline; group 5 rats were diabetic rats administered 50 mg/kg of kola nut extract per day; and group 6 rats were diabetic rats administered 100 mg/kg of kola nut extract per day. Diabetes was induced with 50 mg/kg of STZ. After 3 weeks of administration, the spatial memories of the rats were tested using the Y-maze, followed by assay of Na+/K+-ATPase activity. Results The result shows a significant increase in Na+/K+-ATPase activity of diabetic treated groups (5 and 6) when compared with the diabetic group (4) and a significant increase in Na+/K+-ATPase activity of healthy treated groups (2 and 3) when compared with control. Also, there was a significant increase in spatial memory of the diabetic treated groups when compared with diabetic group. Conclusions This study revealed that kola nut extract has restorative effect on brain Na+/K+-ATPase activities and spatial memory of STZ-induced diabetic female Wistar rats.


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