The above study justifies diosgenin as a promising candidate in diabetes associated complication through its antioxidant and anti-inflammatory activity.

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.

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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

In this study, we have combined the wound-healing properties of two biodegradable polymers, viz., starch and gelatin, and have reinforced their mechanical strength through cross-linking. Further, scaffolds of this polymer combination were used to support an organotypic culture of human skin for wound healing. Human dermal fibroblasts (HDFs) and human epidermal keratinocytes (HEKs) were isolated and were seeded on the scaffolds on days 1 and 7, respectively. The scaffold was then air-lifted to develop a stratified epidermal layer. Hematoxylin and eosin (H&E) staining and immunohistochemical analysis ascertained that the histology of the skin organotypic culture was similar to that of the human skin. For in vivo animal investigations, the scaffolds were transplanted in a full-thickness wound mouse model, as a one-step procedure, wherein the artificial skin substitute showed the presence of well-defined epidermis and formation of stratum basale by day 14. By combining the inherent properties of both the materials, we have synthesized a cost-effective porous scaffold with good mechanical strength and excellent biocompatibility that can be easily adapted for commercial use. The aforementioned scaffold may integrate with the surrounding tissue, accelerate wound closure, and promote tissue reorganization and remodeling.

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.

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.