Epilepsy is a brain disorder characterized by sudden recurrent seizures. Considering the fact that epileptogenesis is a process that affects the quality of life, our goal is to delay the process of epileptogenesis and to increase the latency of epileptic attacks, offering better quality of life to patients. Traditional system of medicines has a promise in some of the medicines, which have been used for the treatment of epilepsy. One such medicinal plant is Eclipta alba (EA). According to Ayurvedic philosophy, the juice of leaves of EA is pounded with garlic and pepper for the treatment of epilepsy. Taking clue from the Ayurvedic system of medicines, we formulated coumarin fraction of EA, namely, coumarin nasal formulation (CNF) for its nasal delivery. CNF was analyzed by using high performance liquid chromatography (HPLC) and ultraviolet absorption spectroscopy for its drug content determination. In vitro drug release studies were performed in simulated nasal electrolyte solution (SNES) maintaining constant pH of 5.5 at 37°C. Irritation by CNF was evaluated using hen’s egg test chorioallantoic membrane (HET-CAM) assay. Formulation was found to be non-irritant in HET-CAM assay. CNF was further assessed in vivo by measuring the progress and attainment of pentylenetetrazole (PTZ) kindling in mice. Neuronal changes were assessed by hematoxylin and eosin (H&E) and Nissl staining technique. Glial fibrillary acidic protein (GFAP) a neuroinflammatory marker and tumor necrosis factor alpha (TNF-α) an inflammatory marker were also measured. CNF (10 mg/kg, nasal route) when given as a pretreatment lowered seizure score and delayed the progression of seizure similar to diazepam. CNF decreased the PTZ induced oxidative damage, TNF-α as well as GFAP levels in the midbrain tissue particularly in hippocampus region. The results suggest that CNF may be a promising therapeutic approach to offer protection from sudden recurrent seizures alone or in combination with current drugs in management of epilepsy.
Diabetic nephropathy affects approximately 20%-40% of diabetes patients worldwide and is the leading cause of end-stage renal failure. Oxidative stress has been identified as a major causative factor in the development and progression of diabetic nephropathy; Nuclear factor erythroid 2-related factor 2 (Nrf2) activation protects the body against oxidative stress by induction of antioxidant enzymes. The renoprotective effect of ethyl ferulate was investigated in diabetes-induced renal injury. Ethyl ferulate was administered orally at three doses (50 mg/kg, 75 mg/kg, and 100 mg/ kg). Metformin (500 mg/kg, p.o.) was used as a standard. Ethyl ferulate treatment decreased serum advanced glycation end products, glycosylated hemoglobin (HbA1c) levels, renal oxidative stress, tumor necrosis factorα (TNFα) level, and kidney hypertrophy index. It restored serum lipid profile, biomarkers of renal function, and mitigated histopathological signs of renal damage. Immunohistochemistry demonstrated higher Nrf2 protein levels in kidney sections of ethyl ferulate-treated rats. These findings suggest that ethyl ferulate ameliorated hyperglycemia-induced oxidative stress by increasing renal Nrf2 levels, thereby preventing diabetes-induced kidney injury. In conclusion, the present study endorses the usefulness of Nrf2 activators, such as ethyl ferulate, as adjuvant therapy for preventing the diabetic nephropathy.How to cite this article: Kaikini AA, Muke S, Peshattiwar V, Bagle S, Dighe V, Sathaye S. Ethyl ferulate, a lipophilic phenylpropanoid, prevents diabetes-associated renal injury in rats by amelioration of hyperglycemia-induced oxidative stress via activation of nuclear factor erythroid 2-related factor 2. J
This study demonstrated the protective effect of phloretin on synaptophysin and adult neuronal proliferating cells in Aβ1-42-injected rats. The encouraging findings highlight the potential of phloretin as a dietary supplement targeting key therapeutic mechanisms in neurodegenerative disorders such as AD.
Background Diabetic retinopathy is a slow progressing complication of diabetes mellitus with multifactorial aetiology affecting approximately 80% of diabetics worldwide. Chronic hyperglycemic milieu of Diabetes induces biochemical changes which contribute to the pathogenesis of Diabetic retinopathy. Objective The present study examined the protective effect of Vasant Kusumakar Ras , an Ayurvedic herbo-mineral formulation, in diabetic retinopathy. Materials and Methods Diabetes was induced in rats by intraperitoneal injection of streptozotocin (45 mg/kg). Rats were kept without any treatment for period of three weeks for induction of Diabetic retinopathy followed by treatment with Vasant Kusumakar Ras (11.25 mg/kg, p.o) for further 5 weeks. Fasting blood glucose levels, lipid profile and HbA1c were determined. Eye tissue homogenates were subjected to biochemical analysis to determine the levels of oxidative stress parameters (superoxide dismutase, catalase, reduced glutathione, lipid peroxidation), vascular endothelial growth factor and aldose reductase activity. Histopathological analysis of retinal tissue was conducted using Hematoxylin and Eosin staining. Results Vasant Kusumakar Ras treatment restored serum lipid profile which was altered in diabetic rats. Treatment with Vasant Kusumakar Ras significantly ameliorated the oxidative stress in eye tissue resulting in decreased lipid peroxidation and increase in endogenous antioxidant levels. Levels of aldose reductase and vascular endothelial growth factor in eye tissue were significantly decreased in Vasant Kusumakar Ras treated rats. Hematoxylin and Eosin staining indicated that the Vasant Kusumakar Ras treatment significantly restored the normal architecture of the retinal tissue. Conclusion Vasant Kusumakar Ras exhibits protective effect and prevents the development of Diabetic retinopathy through its effects on multiple biochemical pathways implicated in pathogenesis of Diabetic retinopathy.
Parkinson’s disease (PD) ranks as second most prevalent neurodegenerative disorder but is devoid of neuroprotective treatment. Approaches with disease modifying ability with symptomatic relief has become an utmost necessity. Further multifactorial nature of PD presents challenges for efficacy evaluation of any potential test compound. The stated study makes an attempt to address these issues by employing a rotenone induced PD model involving a bilateral intranigral stereotactic rotenone injection for evaluation of the neuroprotective efficacy of Daidzein (DZ). DZ a soy isoflavone, is known for its various health benefits viz. immunomodulation, cardiovascular effects etc. In this study, animals after intranigral rotenone (12 μg) injection, were treated with DZ at a dose of 5, 10 and 20 mg/kg for 30 days. The neurobehavioural evaluation comprised of Rota-rod, Open field and Barnes maze test. The biochemical analysis constituting oxidative stress (Reduced glutathione, superoxide dismutase, catalase and lipid peroxidation), inflammation (TNF-α), mitochondrial alteration (complex I activity and biogenesis) was conducted on mid-brain tissue after 30 days of treatment. The SN and striatum was also subjected to immunohistochemical analysis (IHC) for TH positive neurons and Glial Fibrillary Acidic Protein. The analysis revealed significant improvement by daidzein in motor co-ordination and attenuation in cognitive deficits due to rotenone. The biochemical assessment exhibited significant decrement in oxidative stress as well as inflammation. DZ treatment also prevented complex I inhibition and promoted mitochondrial biogenesis eventually contributing to the neuroprotection apparent in IHC. Thus, the results strongly corroborate the neuroprotective potential of DZ against rotenone induced model of PD.
Per WHO, vitamin A deficiency is a systemic disease affecting cells, organs throughout the body. The gradual depletion of vitamin A stores results in xerophthalmia, night blindness, xerosis etc., reversed by vitamin A therapy. Beta-Carotene, a carotenoid, is the precursor of vitamin A, which cannot be synthesized by the human body. Hence beta carotene formulation has gathered considerable attention in the healthcare industry. Hydrophobicity of Beta carotene being a major challenge in the formulation, Zeushygia Life Sciences Pvt. Ltd (Telangana India) developed a novel beta carotene formulation, CaroTex, with enhanced bioavailability. The present study assesses the bioavailability of CaroTex in a rodent model. The animals were divided into 5 groups, Normal Control, Vehicle Control, Standard beta Carotene, Comparator and CaroTex. As rats efficiently convert beta carotene into vitamin A, high dose of beta-carotene (50mg/kg) was given orally for 7 consecutive days. Beta carotene, its metabolic product retinal were measured in rat liver. It was observed that beta carotene concentration in rats fed with CaroTex was about 1.70, 2.55 times higher than Comparator and control respectively whereas the concentration of retinal was the same in all groups. It is evident from this study that novel formulation technology (BioFusion Technology) of CaroTex reflects in relatively higher concentration levels of beta carotene.
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