Exploring the therapeutic potential of Derris elliptica (Wall.) Benth in Streptozotocin-Induced diabetic Rats: Phytochemical characterization and antidiabetic evaluation.

Derris elliptica (Wall.) Benth, a native medicinal plant, has been used to treat diabetes for centuries; however, comprehensive documentation of its bioactive constituents and therapeutic effectiveness is lacking. In this study, we investigated the phytochemical profile and antidiabetic potential of D. elliptica methanolic leaf extract (DEME) in diabetic Sprague Dawley rats induced with streptozotocin (STZ). In normal rats, acute oral toxicity evaluations were conducted, and in STZ-induced rats, antidiabetic properties were investigated. 14 days of oral administration of standard glibenclamide and the extract at 200 and 400 mg/kg body weight to diabetic rodents. Assessed parameters included blood glucose levels, alterations in body weight, biochemical markers, and histological analysis of the pancreas, liver, and kidney. Numerous phytoconstituents were uncovered through qualitative phytochemical assays, 1H NMR, and 1H-13C HSQC screening. Quercetin was identified by 1H NMR characterization, and a ceramide analogue compound was isolated and partially characterized by 1H NMR. There were no indications of toxicity or mortality. The treatment with DEME significantly (p < 0.001) decreased body weight and had a remarkable hypoglycemic effect. Both 200 mg/kg and 400 mg/kg extract concentrations decreased total cholesterol levels significantly (p < 0.01 and p < 0.05, respectively). In addition, glibenclamide and the 400 mg/kg dose of extract increased serum insulin levels substantially (p < 0.05) and decreased total bilirubin, lactic acid dehydrogenase, aspartate aminotransferase, and alanine aminotransferase levels. In addition to glibenclamide, treatment with DEME has exhibited cytoprotective effects and increased insulin secretion, thereby exerting a potent antihyperglycemic effect. These results suggest that D. elliptica may have therapeutic potential for the treatment of diabetes mellitus.

Correction to: Metformin inhibits cardiometabolic syndrome associated cognitive deficits in high fat diet rats.

[This corrects the article DOI: 10.1007/s40200-022-01074-4.].

Dendrimer: An update on recent developments and future opportunities for the brain tumors diagnosis and treatment.

A brain tumor is an uncontrolled cell proliferation, a mass of tissue composed of cells that grow and divide abnormally and appear to be uncontrollable by the processes that normally control normal cells. Approximately 25,690 primary malignant brain tumors are discovered each year, 70% of which originate in glial cells. It has been observed that the blood-brain barrier (BBB) limits the distribution of drugs into the tumour environment, which complicates the oncological therapy of malignant brain tumours. Numerous studies have found that nanocarriers have demonstrated significant therapeutic efficacy in brain diseases. This review, based on a non-systematic search of the existing literature, provides an update on the existing knowledge of the types of dendrimers, synthesis methods, and mechanisms of action in relation to brain tumours. It also discusses the use of dendrimers in the diagnosis and treatment of brain tumours and the future possibilities of dendrimers. Dendrimers are of particular interest in the diagnosis and treatment of brain tumours because they can transport biochemical agents across the BBB to the tumour and into the brain after systemic administration. Dendrimers are being used to develop novel therapeutics such as prolonged release of drugs, immunotherapy, and antineoplastic effects. The use of PAMAM, PPI, PLL and surface engineered dendrimers has proven revolutionary in the effective diagnosis and treatment of brain tumours.

Metformin inhibits cardiometabolic syndrome associated cognitive deficits in high fat diet rats.

Objectives: Glucose intolerance and insulin resistance are hallmarks of metabolic syndrome and lead to Alzheimer's disease (AD). The purpose of this study is to elucidate the neuroprotective effect of metformin through insulin regulation with cardiometabolic and neurotransmitter metabolic enzyme regulation in high-fat, high-sucrose diet and streptozotocin (HFHS-STZ)-induced rats. Methods: Male Wistar rats were treated with metformin (180 mg/kg and 360 mg/kg). STZ (35 mg/kg i.p.) injection was performed on the 14th day of 42 days of HFHS diet treatment. Brain neurotransmitter metabolic enzymes (acetylcholinesterase and monoamine oxidase) were determined along with sodium-potassium ATPase (Na+K+-ATPase). Plasma lipids and homeostasis model assessment of insulin resistance (HOMA-IR) was performed. Mean arterial blood pressure, heart rate and electrocardiogram (QT, QTc and RR intervals) were analysed with PowerLab. Results: Metformin treatment significantly (p < 0.001) reduced the HOMA-IR index and decreased neurotransmitter metabolic enzymes such as AChE and MAO (p < 0.01 and p < 0.05). The lipid profile was significantly (p < 0.001) controlled with cardiometabolic functions. Conclusions: Our investigation revealed that metformin has a remarkable role in regulating brain insulin, vascular system with monoaminergic metabolic enzymes and enhancing synaptic plasticity. Metformin may be a selective early therapeutic agent in metabolic syndrome associated with cognitive decline.

Neuroprotective effects of 1`δ-1`-acetoxyeugenol acetate on Aß(25-35) induced cognitive dysfunction in mice.

The progressive accumulation of amyloid beta (Aß) peptide is neurotoxic and leads to Alzheimer's type dementia. Accumulation of Aß has been associated with dysfunction of hypothalamic-pituitary-adrenal (HPA) axis and elevated pro-inflammatory cytokines. In this study, we investigated the effect of 1`δ-1`-acetoxyeugenol acetate (DAEA), isolated from Alpinia galanga (L.), on Aß(25-35) induced neurodegeneration in mice. Mice were treated with three different doses of DAEA (12.5 mg/kg, 25 mg/kg and 50 mg/kg) for 28 days. Aß(25-35) was injected by intracerebroventricular (i.c.v.) injection on the 15th day of 28 days. Open field, water maze and step-down inhibitory tests were performed on the 27th day to determine the habituation memory, spatial learning, and short- and long-term memory, respectively. Acetylcholinesterase (AChE), Corticosterone, biogenic amines (serotonin and dopamine), tumour necrosis factor-α (TNF-α), and antioxidant parameters such as superoxide dismutase, catalase, glutathione peroxidase and vitamin C were evaluated in brain homogenates after behavioural tests to ascertain the cognitive improvement through neuro-immune-endocrine modulation. The DAEA treatment with 25 mg/kg and 50 mg/kg resulted in significant (p < 0.001) improvement of habituation memory and step-down inhibitory avoidance task. In spatial learning, the cognitive improvement was significantly improved (p < 0.001) by reduction in escape latency. In the biochemical study, the significant (p < 0.001) reduction of AChE indicates the preeminent neuroprotection. Corticosterone and TNF-α were significantly (p < 0.01) reduced and biogenic amines were increased with antioxidant markers, which signify the potential influence of DAEA on neuroprotection. Our investigation revealed that the drug DAEA attenuates stress mediated through the HPA axis and regulates the neuroendocrine and neuroimmune function to improve the cognition. DAEA could be a potential lead candidate for the treatment of neurodegeneration.