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Abstract: Objective: To investigate the protective effects of brown alga Padina boergesenii (P. boergeseii) against carbon tetrachloride (CCl 4) induced oxidative damage and liver fibrosis in rats. Methods: To assess the hepatic damage liver weight, the activities of TBARS level, glutathione, SOD, CAT and GP x in circulation and liver. Results: The group of rats induced with CCl 4 alone (2 mL/kg body weight), showed noticeable increase in the liver weight and TBARS level. Followed by, the level of antioxidant enzymes glutathione peroxidase, Superoxide dismutase and catalase was also significantly (P <0.01) diminished. Where as, the rats pretreated with P. boergesenii (150 mg/kg body weight) modulated the CCl 4 induced liver fibrosis. The level of antioxidant enzymes and lipid peroxidation products was found to be significantly (P <0.01) attenuated to near normal level, when compared with rats induced with CCl 4 alone. In order to assess the role of carotenoids in the relevant activity, total carotenoid content of the extract was analysed and found to be 0.59 mg / g fresh weight (FW). Further, the histopathogical studies provide a supportive evidence for this study to show the protective nature of P. boergesenii. Conclusions: The protective role of brown alga P. boergesenii extract has confirmed its potential activity through its antioxidant sparing actions against CCl 4 i nduced free radical damage. However, the possible mechanism of hepatoprotection is rather speculative at this stage and investigations are underway to isolate and characterize the bioactive compounds from P. boergesenii. [ABSTRACT FROM AUTHOR]

Extracting the essential features and learning the appropriate patterns are the two core character traits of a convolution neural network (CNN). Leveraging the two traits, this research proposes a novel feature extraction framework code-named 'HierbaNetV1' that retrieves and learns effective features from an input image. Originality is brought by addressing the problem of varying-sized region of interest (ROI) in an image by extracting features using diversified filters. For every input sample, 3,872 feature maps are generated with multiple levels of complexity. The proposed method integrates low-level and high-level features thus allowing the model to learn intensive and diversified features. As a follow-up of this research, a crop-weed research dataset termed 'SorghumWeedDataset&#95;Classification' is acquired and created. This dataset is tested on HierbaNetV1 which is compared against pre-trained models and state-of-the-art (SOTA) architectures. Experimental results show HierbaNetV1 outperforms other architectures with an accuracy of 98.06%. An ablation study and component analysis are conducted to demonstrate the effectiveness of HierbaNetV1. Validated against benchmark weed datasets, the study also exhibits that our suggested approach performs well in terms of generalization across a wide variety of crops and weeds. To facilitate further research, HierbaNetV1 weights and implementation are made accessible to the research community on GitHub. To extend the research to practicality, the proposed method is incorporated with a real-time application named HierbaApp that assists farmers in differentiating crops from weeds. Future enhancements for this research are outlined in this article and are currently underway., Competing Interests: The authors declare that they have no competing interests., (© 2024 Michael and Manivasagam.)

Epalrestat (EPS) is a brain penetrant aldose reductase inhibitor, an approved drug currently used for the treatment of diabetic neuropathy. At near-plasma concentration, EPS induces glutathione biosynthesis, which in turn reduces oxidative stress in the neuronal cells. In this study, we found that EPS reduces neurodegeneration by inhibiting reactive oxygen species (ROS)-induced oxidative injury, mitochondrial membrane damage, apoptosis and tauopathy. EPS treatment up to 50 μM did not show any toxic effect on SH-SY5Y cell line (neuroblastoma cells). However, we observed toxic effect at a concentration of 100 μM and above. At 50 μM concentration, EPS showed better antioxidant activity against H 2 O 2 (100 μM)-induced cytotoxicity, ROS formation and mitochondrial membrane damage in retinoic acid-differentiated SH-SY5Y cell line. Furthermore, our study revealed that 50 μM of EPS concentration reduced the glycogen synthase kinase-3 β (GSK3-β) expression and total tau protein level in H 2 O 2 (100 μM)-treated cells. Findings from this study confirms the therapeutic efficacy of EPS on regulating Alzheimer's disease (AD) by regulating GSK3-β and total tau proteins phosphorylation, which helped to restore the cellular viability. This process could also reduce toxic fibrillary tangle formation and disease progression of AD. Therefore, it is our view that an optimal concentration of EPS therapy could decrease AD pathology by reducing tau phosphorylation through regulating the expression level of GSK3-β.

The original version of this article unfortunately contains an error in Figs. 8 and 9.

Polyphenols are shown to protect from or delay the progression of chronic neurodegenerative diseases. Mitochondrial dysfunction plays a key role in the pathogenesis of Parkinson's disease (PD). This study was aims to gain insight into the role of ahydroalcoholic extract of cocoa (standardised for epicatechin content) on mitochondrial biogenesis in MPP + intoxicated human neuroblastoma cells (SHSY5Y). The effects of cocoa on PPARγ, PGC1α, Nrf2 and TFAM protein expression and mitochondrial membrane potential were evaluated. A pre-exposure to cocoa extract decreased reactive oxygen species formation and restored mitochondrial membrane potential. The cocoa extract was found to up-regulate the expression of PPARγ and the downstream signalling proteins PGC1α, Nrf2 and TFAM. It increased the expression of the anti-apoptotic protein BCl2 and increased superoxide dismutase activity. Further, the cocoa extract down-regulated the expression of mitochondria fission 1 (Fis1) and up-regulated the expression of mitochondria fusion 2 (Mfn2) proteins, suggesting an improvement in mitochondrial functions in MPP + intoxicated cells upon treatment with cocoa. Interestingly, cocoa up-regulates the expression of tyrosine hydroxylase, the rate limiting enzyme in dopamine synthesis. No change in the expression of PPARγ on treatment with cocoa extract was observed when the cells were pre-treated with PPARγ antagonist GW9662. This data suggests that cocoa mediates mitochondrial biogenesis via a PPARγ/PGC1α dependent signalling pathway and also has the ability to improve dopaminergic functions by increasing tyrosine hydroxylase expression. Based on our data, we propose that a cocoa bean extract and products thereof could be used as potential nutritional supplements for neuroprotection in PD.

Autism spectrum disorder (ASD) is a developmental disorder that influences communication and behavior. Numerous researches propose that genes can act together with manipulations from the environment to affect development in ways that lead to ASD. The broad range of issues facing people with ASD means that there is no single proper drug and treatment for ASD. Numerous shortcomings associated with the present conventional therapeutic strategies have forced researchers to venture into alternative natural sources for effective compounds. The marine environment has emerged as an alternate search environment due to its versatile conditions where organisms employ various biodefense mechanisms for their survival. Ascidians are an excellent source for unique bioactive compounds with nutritive and therapeutic content and it still holds credit for being an underused source from marine animals. Bioactive compounds isolated from ascidians have various commendable biomedical applications due to their unique chemical structures. The present chapter will focus on the potential of bioactive compounds derived from ascidians for the treatment of the neurologic disorder-ASD.

Autism spectrum disorder (ASD) is a heterogeneous group of neurodevelopmental disorders with poorly understood etiology that are defined exclusively on the basis of behavioral observations. This disorder has been linked to increased levels of oxidative stress and lower antioxidant capacity. Oxidative stress in autism has been studied at the membrane level and also by measuring products of lipid peroxidation, detoxifying agents (such as glutathione), and antioxidants involved in the defense system against reactive oxygen species (ROS). Several studies have suggested alterations in the activities of antioxidant enzymes such as superoxide dismutase, glutathione peroxidase, and catalase in autism. Additionally, altered glutathione levels and homocysteine/methionine metabolism, increased inflammation, excitotoxicity, as well as mitochondrial and immune dysfunction have been suggested in autism. Moreover, environmental and genetic risk factors may intensify vulnerability to oxidative stress in autism. Collectively, these studies suggest increased oxidative stress in autism that may contribute to the development of this disease both in terms of pathogenesis and clinical symptoms. Antioxidant supplementation, or ways to improve the altered metabolite levels in the interconnected transmethylation and transsulfuration pathways, has been associated with decreased autistic behaviors and severity. This chapter provides a conceptual framework on oxidative stress and antioxidants utility. These types of interventions should be further studied in order to determine their effectiveness at improving metabolic imbalances.

Autism is a complex neurodevelopmental disorder that is evident in early childhood and can persist throughout the entire life. The disease is basically characterized by hurdles in social interaction where the individuals demonstrate repetitive and stereotyped interests or patterns of behavior. A wide number of neuroanatomical studies with autistic patients revealed alterations in brain development which lead to diverse cellular and anatomical processes including atypical neurogenesis, neuronal migration, maturation, differentiation, and degeneration. Special education programs, speech and language therapy, have been employed for the amelioration of behavioral deficits in autism. Although commonly prescribed antidepressants, antipsychotics, anticonvulsants, and stimulants have revealed satisfactory responses in autistic individuals, adverse side effects and increased risk of several other complications including obesity, dyslipidemia, diabetes mellitus, thyroid disorders, etc. have compelled the researchers to turn their attention toward herbal remedies. Alternative approaches with natural compounds are on continuous clinical trial to confirm their efficacy and to understand their potential in autism treatment. This chapter aims to cover the major plant-based natural products which hold promising outcomes in the field of reliable therapeutic interventions for autism.