Dietary Co-supplements attenuate the chronic unpredictable mild stress-induced depression in mice.

Does it make a difference what we eat when it comes to our mental health? Food and nutrients are essential not only for human biology and physical appearance but also for mental and emotional well-being. There has been a significant increase in the favourable effects of dietary supplements in the treatment of depressive state in the latest days. Co-supplements which can be a great contribution in the management of depression from the future perspective and might help to reduce standard anti-depressant drug doses, which can be a strategic way to reduce the side effect of standard anti-depressants drugs. This study was designed to evaluate and compare the anti-depressant effects of cholecalciferol-D3 (V.D3), n-3 polyunsaturated fatty acid (PUFA), and a combination of V.D3 + n-3 PUFA with fluoxetine treatment in chronic unpredictable mild stress (CUMS) induced depression in the mice model. We established CUMS depressant mice model and treated CUMS mice with V.D3, n-3 PUFA, and a combination of V.D3 + n-3 PUFA with fluoxetine. Behavioral changes were measured by the forced swim and tail suspension test. Oxidative stress markers and anti-depressant activity were assessed through parameters such as superoxide dismutase, reduced glutathione, lipid peroxidation, and serum corticosterone levels. Additionally, we measured the levels of neurotransmitters dopamine and serotonin. CUMS induced mice displayed depressive-like behaviours. Moreover, cholecalciferol-D3, n-3 PUFA, and a combination of Cholecalciferol-D3 + n-3 PUFA with fluoxetine treatment attenuated the depressive-like behaviour in CUMS mice accompanied with suppression of oxidative stress markers by up-regulated the expression of an antioxidant signalling pathway. The results suggested that treatment of cholecalciferol-D3, n-3 PUFA, and a combination of Cholecalciferol-D3 + n-3 PUFA with fluoxetine significantly ameliorated depressive-like behaviours in CUMS induced depression in mice. To delve further into the implications of these findings, future studies could explore the specific molecular mechanisms underlying the observed effects on oxidative stress markers and the antioxidant signaling pathway. This could provide valuable insights into the potential of dietary supplements in the management of depression and help in reducing the reliance on conventional antidepressant medications, thus improving the overall quality of treatment for this prevalent mental health condition.

Beyond Glucose: The Dual Assault of Oxidative and ER Stress in Diabetic Disorders.

Diabetes mellitus, a prevalent global health concern, is characterized by hyperglycemia. However, recent research reveals a more intricate landscape where oxidative stress and endoplasmic reticulum (ER) stress orchestrate a dual assault, profoundly impacting diabetic disorders. This review elucidates the interplay between these two stress pathways and their collective consequences on diabetes. Oxidative stress emanates from mitochondria, where reactive oxygen species (ROS) production spirals out of control, leading to cellular damage. We explore ROS-mediated signaling pathways, which trigger ß-cell dysfunction, insulin resistance, and endothelial dysfunction the quintessential features of diabetes. Simultaneously, ER stress unravels, unveiling how protein folding disturbances activate the unfolded protein response (UPR). We dissect the UPR's dual role, oscillating between cellular adaptation and apoptosis, significantly influencing pancreatic ß-cells and peripheral insulin-sensitive tissues. Crucially, this review exposes the synergy between oxidative and ER stress pathways. ROS-induced UPR activation and ER stress-induced oxidative stress create a detrimental feedback loop, exacerbating diabetic complications. Moreover, we spotlight promising therapeutic strategies that target both stress pathways. Antioxidants, molecular chaperones, and novel pharmacological agents offer potential avenues for diabetes management. As the global diabetes burden escalates, comprehending the dual assault of oxidative and ER stress is paramount. This review not only unveils the intricate molecular mechanisms governing diabetic pathophysiology but also advocates a holistic therapeutic approach. By addressing both stress pathways concurrently, we may forge innovative solutions for diabetic disorders, ultimately alleviating the burden of this pervasive health issue.

Combination of Ocimum sanctum extract and Levetiracetam ameliorates cognitive dysfunction and hippocampal architecture in rat model of Alzheimer's disease.

Alzheimer's disease (AD) is the most common neurodegenerative disease which affects more than 40 million people worldwide with progressive loss of memory and cognitive functions. It is reported, persistent AD is also one of the main causes of epilepsy in elders and comorbidity of both these will contribute to worsening the health status of AD patients. Recently, herbal plants with potent neuroprotective and antioxidant properties were used for increasing the quality of life in neurodegenerative disease patients. The present study was conceptualized to access the protective effect of Ocimum sanctum extract (OSE) and Levetiracetam (LEV) and their combination (OSE+LEV) against AD and epilepsy associated with AD in the rat AD model. AD was induced in aged male Wistar albino rats with Amyloid-ß (Aß) by intracerebroventricular administration. The results reveal, treatment with OSE, LEV and OSE+LEV significantly reversed the memory impairment, increases the BDNF expressions and decreases AChE activity in Aß induced AD animals. Expression of A-ß and p-tau in the hippocampus was significantly reduced in treatment group when compared to the control animals. Treatment with OSE and OSE+LEV also restored the hippocampal architecture by ameliorating the neuronal count in CA1, CA3 and DG regions. It also observed that treatment has decreased the excitoneurotoxicity evidenced by decreased glutamate and increased GABA levels and thus provided protection against epilepsy. Treatment groups also exhibited a potent antioxidant activity when tested endogenous antioxidant enzymes SOD, GSH and LPO in the brain hippocampus. Our findings provide evidence for use of OSE, LEV and OSE+LEV against AD and epilepsy associated with AD in Aß induced AD animal model. However, further clinical studies are required to prove the use of OSE, LEV and OSE+LEV in the management of AD and AD-associated epilepsy in human volunteers.

Antioxidant and hepatoprotective activity of ethanolic and aqueous extracts of Momordica dioica Roxb. leaves.

In present study, the hepatoprotective activity of ethanolic and aqueous extracts of Momordica dioica Roxb. leaves were evaluated against carbon tetrachloride (CCl4) induced hepatic damage in rats. The extracts at dose of 200mg/kg were administered orally once daily. The substantially elevated serum enzymatic levels of serum glutamate oxaloacetate transaminase (AST), serum glutamate pyruvate transaminase (ALT), serum alkaline phosphatase (SALP) and total bilirubin were restored towards normalization significantly by the extracts. Silymarin was used as standard reference and exhibited significant hepatoprotective activity against carbon tetrachloride induced haptotoxicity in rats. The biochemical observations were supplemented with histopathological examination of rat liver sections. The results of this study strongly indicate that Momordica dioica Roxb. leaves have potent hepatoprotective action against carbon tetrachloride induced hepatic damage in rats. Ethanolic extract was found more potent hepatoprotective. Meanwhile, in vivo antioxidant and free radical scavenging activities were also screened which were positive for both ethanolic and aqueous extracts. This study suggests that possible mechanism of this activity may be due to free radical-scavenging and antioxidant activities which may be due to the presence of flavonoids in the extracts.