Synthesis of Silver Nanoparticles Using Camellia sinensis Leaf Extract: Promising Particles for the Treatment of Cancer and Diabetes.

Both diabetes and cancer pose significant threats to public health. To overcome these challenges, nanobiotechnology offers innovative solutions for the treatment of these diseases. However, the synthesis of nanoparticles can be complex, costly and environmentally toxic. Therefore, in this study, we successfully synthesized Camellia sinensis silver nanoparticles (CS-AgNPs) biologically from methanolic leaf extract of C. sinensis and as confirmed by the visual appearance which exhibited strong absorption at 456 nm in UV-visible spectroscopy. The fourier transform infrared spectroscopy (FTIR) analysis revealed that phytochemicals of C. sinensis were coated with AgNPs. Scanning electron microscopy (SEM) analysis showed the spherical shape of CS-AgNPs, with a size of 15.954 nm, while X-ray diffraction spectrometry (XRD) analysis detected a size of 20.32 nm. Thermogravimetric analysis (TGA) indicated the thermal stability of CS-AgNPs. The synthesized CS-AgNPs significantly inhibited the ehrlich ascites carcinoma (EAC) cell growth with 53.42±1.101 %. The EAC cell line induced mice exhibited increased level of the serum aspartate aminotransferase (AST), alanine transaminase (ALT), and alkaline phosphatase (ALP), however this elevated serum parameter significantly reduced and controlled by the treatment with CS-AgNPs. Moreover, in a streptozotocin-induced diabetic mice model, CS-AgNPs greatly reduced blood glucose, total cholesterol, triglyceride, low-density lipoprotein (LDL) and creatinine levels. These findings highlight that the synthesized CS-AgNPs have significant anticancer and antidiabetic activities that could be used as promising particles for the treatment of these major diseases. However, pre-clinical and clinical trial should be addressed before use this particles as therapeutics agents.

Effect of water quality parameters and climatic influences on reproductive phenology of Macrognathus pancalus in wetland ecosystem: recommending a long-term management approach and conservation policy.

The study conducted an investigation into the reproductive biology of M. pancalus and assessed the influence of water quality parameters and environmental factors on the spawning pattern within the Gajner Beel ecosystem in Bangladesh. A total of 1218 individuals of M. pancalus (46.39% males and 53.61% females) were collected monthly from the Gajner Beel during January to December 2018 using various fishing gears. The total length (TL) of each individual was measured using digital slide calipers, and the whole body weight (BW) was measured using an electronic balance. Fulton's conditions factor (KF) showed significant differences between males and females. The calculated Lm were 11.11 cm, 11.30 cm, and 11.10 cm based on maximum length, gonadosomatic index (GSI), and the logistic model. The spawning season extended from May through August, with June and July being peak months. The average total fecundity was 1495.52 ± 840.24, with a range of 370 to 4069. During peak spawning season, the average temperature and rainfall were 27°C and 370 mm, respectively. Rainfall, dissolved oxygen, total alkalinity, and pH all had a significant (p < 0.01) positive effect whereas temperature and TDS all had a significant (p > 0.01) negative effect on GSI. Annual air temperature in the study area increased by 0.053 °C/year, with a regression coefficient value (r2 = 0.1695), while annual mean rainfall decreased by 5.97mm/year (r2 = 0.076). This research will contribute to the development of conservation and management approaches of Mastacembelidae fish in relation to current climate variability in sub-tropical waters.

Amentoflavone derivatives significantly act towards the main protease (3CLPRO/MPRO) of SARS-CoV-2: in silico admet profiling, molecular docking, molecular dynamics simulation, network pharmacology.

SARS-CoV-2 is the foremost culprit of the novel coronavirus disease 2019 (nCoV-19 and/or simply COVID-19) and poses a threat to the continued life of humans on the planet and create pandemic issue globally. The 3-chymotrypsin-like protease (MPRO or 3CLPRO) is the crucial protease enzyme of SARS-CoV-2, which directly involves the processing and release of translated non-structural proteins (nsps), and therefore involves the development of virus pathogenesis along with outbreak the forecasting of COVID-19 symptoms. Moreover, SARS-CoV-2 infections can be inhibited by plant-derived chemicals like amentoflavone derivatives, which could be used to develop an anti-COVID-19 drug. Our research study is designed to conduct an in silico analysis on derivatives of amentoflavone (isoginkgetin, putraflavone, 4''''''-methylamentoflavone, bilobetin, ginkgetin, sotetsuflavone, sequoiaflavone, heveaflavone, kayaflavone, and sciadopitysin) for targeting the non-structural protein of SARS-CoV-2, and subsequently further validate to confirm their antiviral ability. To conduct all the in silico experiments with the derivatives of amentoflavone against the MPRO protein, both computerized tools and online servers were applied; notably the software used is UCSF Chimera (version 1.14), PyRx, PyMoL, BIOVIA Discovery Studio tool (version 4.5), YASARA (dynamics simulator), and Cytoscape. Besides, as part of the online tools, the SwissDME and pKCSM were employed. The research study was proposed to implement molecular docking investigations utilizing compounds that were found to be effective against the viral primary protease (MPRO). MPRO protein interacted strongly with 10 amentoflavone derivatives. Every time, amentoflavone compounds outperformed the FDA-approved antiviral medicine that is currently underused in COVID-19 in terms of binding affinity (- 8.9, - 9.4, - 9.7, - 9.1, - 9.3, - 9.0, - 9.7, - 9.3, - 8.8, and - 9.0 kcal/mol, respectively). The best-selected derivatives of amentoflavone also possessed potential results in 100 ns molecular dynamic simulation (MDS) validation. It is conceivable that based on our in silico research these selected amentoflavone derivatives more precisely 4''''''-methylamentoflavone, ginkgetin, and sequoiaflavone have potential for serving as promising lead drugs against SARS-CoV-2 infection. In consequence, it is recommended that additional in vitro as well as in vivo research studies have to be conducted to support the conclusions of this current research study.

Natural flavonoids effectively block the CD81 receptor of hepatocytes and inhibit HCV infection: a computational drug development approach.

Hepatitis C virus (HCV) infection is a major public health concern, and almost two million people are infected per year globally. This is occurred by the diverse spectrum of viral genotypes, which are directly associated with chronic liver disease (fibrosis, and cirrhosis). Indeed, the viral genome encodes three principal proteins as sequentially core, E1, and E2. Both E1 and E2 proteins play a crucial role in the attachment of the host system, but E2 plays a more fundamental role in attachment. The researchers have found the "E2-CD81 complex" at the entry site, and therefore, CD81 is the key receptor for HCV entrance in both humans, and chimpanzees. So, the researchers are trying to block the host CD81 receptor and halt the virus entry within the cellular system via plant-derived compounds. Perhaps that is why the current research protocol is designed to perform an in silico analysis of the flavonoid compounds for targeting the tetraspanin CD81 receptor of hepatocytes. To find out the best flavonoid compounds from our library, web-based tools (Swiss ADME, pKCSM), as well as computerized tools like the PyRx, PyMOL, BIOVIA Discovery Studio Visualizer, Ligplot+ V2.2, and YASARA were employed. For molecular docking studies, the flavonoid compounds docked with the targeted CD81 protein, and herein, the best-outperformed compounds are Taxifolin, Myricetin, Puerarin, Quercetin, and (-)-Epicatechin, and outstanding binding affinities are sequentially - 7.5, - 7.9, - 8.2, - 8.4, and - 8.5 kcal/mol, respectively. These compounds have possessed more interactions with the targeted protein. To validate the post docking data, we analyzed both 100 ns molecular dynamic simulation, and MM-PBSA via the YASARA simulator, and finally finds the more significant outcomes. It is concluded that in the future, these compounds may become one of the most important alternative antiviral agents in the fight against HCV infection. It is suggested that further in vivo, and in vitro research studies should be done to support the conclusions of this in silico research workflow.

A Comprehensive Analysis and Anti-Cancer Activities of Quercetin in ROS-Mediated Cancer and Cancer Stem Cells.

Reactive oxygen species (ROS) induce carcinogenesis by causing genetic mutations, activating oncogenes, and increasing oxidative stress, all of which affect cell proliferation, survival, and apoptosis. When compared to normal cells, cancer cells have higher levels of ROS, and they are responsible for the maintenance of the cancer phenotype; this unique feature in cancer cells may, therefore, be exploited for targeted therapy. Quercetin (QC), a plant-derived bioflavonoid, is known for its ROS scavenging properties and was recently discovered to have various antitumor properties in a variety of solid tumors. Adaptive stress responses may be induced by persistent ROS stress, allowing cancer cells to survive with high levels of ROS while maintaining cellular viability. However, large amounts of ROS make cancer cells extremely susceptible to quercetin, one of the most available dietary flavonoids. Because of the molecular and metabolic distinctions between malignant and normal cells, targeting ROS metabolism might help overcome medication resistance and achieve therapeutic selectivity while having little or no effect on normal cells. The powerful bioactivity and modulatory role of quercetin has prompted extensive research into the chemical, which has identified a number of pathways that potentially work together to prevent cancer, alongside, QC has a great number of evidences to use as a therapeutic agent in cancer stem cells. This current study has broadly demonstrated the function-mechanistic relationship of quercetin and how it regulates ROS generation to kill cancer and cancer stem cells. Here, we have revealed the regulation and production of ROS in normal cells and cancer cells with a certain signaling mechanism. We demonstrated the specific molecular mechanisms of quercetin including MAPK/ERK1/2, p53, JAK/STAT and TRAIL, AMPKα1/ASK1/p38, RAGE/PI3K/AKT/mTOR axis, HMGB1 and NF-κB, Nrf2-induced signaling pathways and certain cell cycle arrest in cancer cell death, and how they regulate the specific cancer signaling pathways as long-searched cancer therapeutics.

Statistical Bioinformatics to Uncover the Underlying Biological Mechanisms That Linked Smoking with Type 2 Diabetes Patients Using Transcritpomic and GWAS Analysis.

Type 2 diabetes (T2D) is a chronic metabolic disease defined by insulin insensitivity corresponding to impaired insulin sensitivity, decreased insulin production, and eventually failure of beta cells in the pancreas. There is a 30-40 percent higher risk of developing T2D in active smokers. Moreover, T2D patients with active smoking may gradually develop many complications. However, there is still no significant research conducted to solve the issue. Hence, we have proposed a highthroughput network-based quantitative pipeline employing statistical methods. Transcriptomic and GWAS data were analysed and obtained from type 2 diabetes patients and active smokers. Differentially Expressed Genes (DEGs) resulted by comparing T2D patients' and smokers' tissue samples to those of healthy controls of gene expression transcriptomic datasets. We have found 55 dysregulated genes shared in people with type 2 diabetes and those who smoked, 27 of which were upregulated and 28 of which were downregulated. These identified DEGs were functionally annotated to reveal the involvement of cell-associated molecular pathways and GO terms. Moreover, protein-protein interaction analysis was conducted to discover hub proteins in the pathways. We have also identified transcriptional and post-transcriptional regulators associated with T2D and smoking. Moreover, we have analysed GWAS data and found 57 common biomarker genes between T2D and smokers. Then, Transcriptomic and GWAS analyses are compared for more robust outcomes and identified 1 significant common gene, 19 shared significant pathways and 12 shared significant GOs. Finally, we have discovered protein-drug interactions for our identified biomarkers.

Prospects of Marine Sterols against Pathobiology of Alzheimer's Disease: Pharmacological Insights and Technological Advances.

Alzheimer's disease (AD) is a degenerative brain disorder characterized by a progressive decline in memory and cognition, mostly affecting the elderly. Numerous functional bioactives have been reported in marine organisms, and anti-Alzheimer's agents derived from marine resources have gained attention as a promising approach to treat AD pathogenesis. Marine sterols have been investigated for several health benefits, including anti-cancer, anti-obesity, anti-diabetes, anti-aging, and anti-Alzheimer's activities, owing to their anti-inflammatory and antioxidant properties. Marine sterols interact with various proteins and enzymes participating via diverse cellular systems such as apoptosis, the antioxidant defense system, immune response, and cholesterol homeostasis. Here, we briefly overview the potential of marine sterols against the pathology of AD and provide an insight into their pharmacological mechanisms. We also highlight technological advances that may lead to the potential application of marine sterols in the prevention and therapy of AD.

Role of Insulin in Health and Disease: An Update.

Insulin is a polypeptide hormone mainly secreted by ß cells in the islets of Langerhans of the pancreas. The hormone potentially coordinates with glucagon to modulate blood glucose levels; insulin acts via an anabolic pathway, while glucagon performs catabolic functions. Insulin regulates glucose levels in the bloodstream and induces glucose storage in the liver, muscles, and adipose tissue, resulting in overall weight gain. The modulation of a wide range of physiological processes by insulin makes its synthesis and levels critical in the onset and progression of several chronic diseases. Although clinical and basic research has made significant progress in understanding the role of insulin in several pathophysiological processes, many aspects of these functions have yet to be elucidated. This review provides an update on insulin secretion and regulation, and its physiological roles and functions in different organs and cells, and implications to overall health. We cast light on recent advances in insulin-signaling targeted therapies, the protective effects of insulin signaling activators against disease, and recommendations and directions for future research.

Multifarious roles of mTOR signaling in cognitive aging and cerebrovascular dysfunction of Alzheimer's disease.

Age-related cognitive failure is a main devastating incident affecting even healthy people. Alzheimer's disease (AD) is the utmost common form of dementia among the geriatric community. In the pathogenesis of AD, cerebrovascular dysfunction is revealed before the beginning of the cognitive decline. Mounting proof shows a precarious impact of cerebrovascular dysregulation in the development of AD pathology. Recent studies document that the mammalian target of rapamycin (mTOR) acts as a crucial effector of cerebrovascular dysregulation in AD. The mTOR contributes to brain vascular dysfunction and subsequence cerebral blood flow deficits as well as cognitive impairment. Furthermore, mTOR causes the blood-brain barrier (BBB) breakdown in AD models. Inhibition of mTOR hyperactivity protects the BBB integrity in AD. Furthermore, mTOR drives cognitive defect and cerebrovascular dysfunction, which are greatly prevalent in AD, but the central molecular mechanisms underlying these alterations are obscure. This review represents the crucial and current research findings regarding the role of mTOR signaling in cognitive aging and cerebrovascular dysfunction in the pathogenesis of AD.

Neuroprotective Potentials of Marine Algae and Their Bioactive Metabolites: Pharmacological Insights and Therapeutic Advances.

Beyond their significant contribution to the dietary and industrial supplies, marine algae are considered to be a potential source of some unique metabolites with diverse health benefits. The pharmacological properties, such as antioxidant, anti-inflammatory, cholesterol homeostasis, protein clearance and anti-amyloidogenic potentials of algal metabolites endorse their protective efficacy against oxidative stress, neuroinflammation, mitochondrial dysfunction, and impaired proteostasis which are known to be implicated in the pathophysiology of neurodegenerative disorders and the associated complications after cerebral ischemia and brain injuries. As was evident in various preclinical studies, algal compounds conferred neuroprotection against a wide range of neurotoxic stressors, such as oxygen/glucose deprivation, hydrogen peroxide, glutamate, amyloid ß, or 1-methyl-4-phenylpyridinium (MPP+) and, therefore, hold therapeutic promise for brain disorders. While a significant number of algal compounds with promising neuroprotective capacity have been identified over the last decades, a few of them have had access to clinical trials. However, the recent approval of an algal oligosaccharide, sodium oligomannate, for the treatment of Alzheimer's disease enlightened the future of marine algae-based drug discovery. In this review, we briefly outline the pathophysiology of neurodegenerative diseases and brain injuries for identifying the targets of pharmacological intervention, and then review the literature on the neuroprotective potentials of algal compounds along with the underlying pharmacological mechanism, and present an appraisal on the recent therapeutic advances. We also propose a rational strategy to facilitate algal metabolites-based drug development.

Oxyresveratrol activates parallel apoptotic and autophagic cell death pathways in neuroblastoma cells.

BACKGROUND: Drug resistance from apoptosis is a challenging issue with different cancer types, and there is an interest in identifying other means of inducing cytotoxicity. Here, treatment of neuroblastoma cells with oxyresveratrol (OXYRES), a natural antioxidant, led to dose-dependent cell death and increased autophagic flux along with activation of caspase-dependent apoptosis. METHODS: For cell viability, we performed the CCK-8 assay. Protein expression changes were with Western blot and immunocytochemistry. Silencing of proteins was with siRNA. The readouts for cell cycle, mitochondria membrane potential, caspase-3, autophagy and apoptosis were performed with flow cytometry. RESULTS: Phosphorylation of p38 MAPK increased with OXYRES treatment and inhibition of p38 reduced autophagy and cell death from OXYRES. In contrast, PI3K/AKT/mTOR signaling decreased in the target cells with OXYRES and inhibition of PI3K or mTOR enhanced OXYRES-mediated cytotoxicity with increased levels of autophagy. Modulation of either of the apoptosis and autophagy flux pathways affected the extent of cell death by OXYRES, but did not affect the indicators of these pathways with respect to each other. Both pathways were independent of ROS generation or p53 activation. CONCLUSION: OXYRES led to cell death from autophagy, which was independent of apoptosis induction. The OXYRES effects were due to changes in the activity levels of p38 MAPK and PI3K/AKT/mTOR. GENERAL SIGNIFICANCE: With two independent and parallel pathways for cytotoxicity induction in target cells, this study puts forward a potential utility for OXYRES or the pathways it represents as novel means of inducing cell death in neuroblastoma cells.

Recent Treatment Strategies and Molecular Pathways in Resistance Mechanisms of Antiangiogenic Therapies in Glioblastoma.

Malignant gliomas present great difficulties in treatment, with little change over the past 30 years in the median survival time of 15 months. Current treatment options include surgery, radiotherapy (RT), and chemotherapy. New therapies aimed at suppressing the formation of new vasculature (antiangiogenic treatments) or destroying formed tumor vasculature (vascular disrupting agents) show promise. This study summarizes the existing knowledge regarding the processes by which glioblastoma (GBM) tumors acquire resistance to antiangiogenic treatments. The discussion encompasses the activation of redundant proangiogenic pathways, heightened tumor cell invasion and metastasis, resistance induced by hypoxia, creation of vascular mimicry channels, and regulation of the tumor immune microenvironment. Subsequently, we explore potential strategies to overcome this resistance, such as combining antiangiogenic therapies with other treatment methods, personalizing treatments for each patient, focusing on new therapeutic targets, incorporating immunotherapy, and utilizing drug delivery systems based on nanoparticles. Additionally, we would like to discuss the limitations of existing methods and potential future directions to enhance the beneficial effects of antiangiogenic treatments for patients with GBM. Therefore, this review aims to enhance the research outcome for GBM and provide a more promising opportunity by thoroughly exploring the mechanisms of resistance and investigating novel therapeutic strategies.

Drug Target to Alleviate Mitochondrial Dysfunctions in Alzheimer's Disease: Recent Advances and Therapeutic Implications.

Alzheimer's disease (AD) is a severe progressive neurodegenerative condition associated with neuronal damage and reduced cognitive function that primarily affects the aged worldwide. While there is increasing evidence suggesting that mitochondrial dysfunction is one of the most significant factors contributing to AD, its accurate pathobiology remains unclear. Mitochondrial bioenergetics and homeostasis are impaired and defected during AD pathogenesis. However, the potential of mutations in nuclear or mitochondrial DNA encoding mitochondrial constituents to cause mitochondrial dysfunction has been considered since it is one of the intracellular processes commonly compromised in early AD stages. Additionally, electron transport chain dysfunction and mitochondrial pathological protein interactions are related to mitochondrial dysfunction in AD. Many mitochondrial parameters decline during aging, causing an imbalance in reactive oxygen species (ROS) production, leading to oxidative stress in age-related AD. Moreover, neuroinflammation is another potential causative factor in AD-associated mitochondrial dysfunction. While several treatments targeting mitochondrial dysfunction have undergone preclinical studies, few have been successful in clinical trials. Therefore, this review discusses the molecular mechanisms and different therapeutic approaches for correcting mitochondrial dysfunction in AD, which have the potential to advance the future development of novel drug-based AD interventions.

Reconfigurable image processing metasurfaces with phase-change materials.

Optical metasurfaces have enabled analog computing and image processing within sub-wavelength footprints, and with reduced power consumption and faster speeds. While various image processing metasurfaces have been demonstrated, most of the considered devices are static and lack reconfigurability. Yet, the ability to dynamically reconfigure processing operations is key for metasurfaces to be used within practical computing systems. Here, we demonstrate a passive edge-detection metasurface operating in the near-infrared regime whose response can be drastically modified by temperature variations smaller than 10 °C around a CMOS-compatible temperature of 65 °C. Such reconfigurability is achieved by leveraging the insulator-to-metal phase transition of a thin layer of vanadium dioxide, which strongly alters the metasurface nonlocal response. Importantly, this reconfigurability is accompanied by performance metrics-such as numerical aperture, efficiency, isotropy, and polarization-independence - close to optimal, and it is combined with a simple geometry compatible with large-scale manufacturing. Our work paves the way to a new generation of ultra-compact, tunable and passive devices for all-optical computation, with potential applications in augmented reality, remote sensing and bio-medical imaging.

Highly efficient recyclable bismuth nanocatalysts fabricated using a facile one-step aqueous method for faster reduction of azo dye contaminants.

Easily accessible robust synthesis of metallic nanoparticles (NPs) and their colloidal stabilization via successive surface functionalization with desired molecules are crucial for catalytic applications. In this research, tannic acid (TA)-functionalized bismuth (Bi)-based novel NPs were prepared via a simple in situ aqueous reduction of Bi3+ ions for the catalytic reduction of azo groups. The synthesis, morphology, and structure of Bi/TANPs were confirmed through spectroscopic, electron microscopic and X-ray diffraction analyses. The Bi/TANPs comprise Bi, carbon, oxygen and sodium as building components and possess a high negative surface charge of -58 mV, colloidal dispersity, thermal stability and crystalline structure. The Bi/TANPs are almost spherical shaped with an average diameter of 33 nm. The surface of the catalyst is mesoporous with a high specific surface area of 267 m2 g-1. The designed Bi/TANPs exhibit pH-specific affinity for azo dye molecules and reduced azo moieties in the presence of aqueous NaBH4 without requiring any hydrogen gas supply. The catalytic reduction efficiencies of Bi/TANPs against methylene blue and Congo red are almost 100%. These reduction reactions are very fast owing to the presence of TA moieties on the catalyst surface, which facilitate direct electron transfer to azo groups, and follow a pseudo-first-order kinetic model. The catalyst is mechanically recyclable, and shows a minimal loss (<3%) of its initial efficiency until the fifth cycle. This study not only developed an efficient catalyst for the remediation of azo dye-contaminated water, but also offers novel insights into the synergistic effects of TA and glycerin on the reduction mechanism of aqueous Bi3+ ions and the concomitant colloidal stabilization of Bi NPs.

A systematic review on green synthesis of silver nanoparticles using plants extract and their bio-medical applications.

Nanoparticles have recently become considered as a crucial player in contemporary medicine, with therapeutic uses ranging from contrast agents in imaging to carriers for the transport of drugs and genes into a specific target. Nanoparticles have the ability to have more precise molecular interactions with the human body in order to target specific cells and tissues with minimal adverse effects and maximal therapeutic outcomes. With the least number of side effects and the greatest possible therapeutic benefit, nanoparticles can target particular cells and tissues through more precise molecular interactions with the human body. The majority of global public health problems are now treated with green synthesized silver nanoparticles (AgNPs), which substantially affect the fundamental structure of DNA and proteins and thus display their antimicrobial action. AgNPs can inhibit the proliferation of tumor cells and induce oxidative stress. By inhibiting vascular endothelial growth factor (HIF)-1, pro-inflammatory mediators generated by silver nanoparticles are reduced, mucin hypersecretion is lessened, and gene activity is subsequently regulated to prevent infections. The biogenic synthesis of silver nanoparticles (AgNPs) using various plants and their applications in antibacterial, antifungal, antioxidant, anticancer, anti-inflammatory, and antidiabetic activities have been extensively discussed in this article. Also, because only natural substances are utilized in the manufacturing process, the particles that are created naturally are coated, stabilized, and play a vital role in these biomedical actions. The characterization of AgNPs, possibility of preparing AgNPSs with different shapes using biological method and their impact on functions and toxicities, impact of size, shape and other properties on AgNPs functions and toxicity profiles, limitations, and future prospects of green-mediated AgNPs have also been reported in this study. The major goal of this study is to provide readers with a comprehensive, informed, and up-to-date summary of the various AgNPs production and characterization methods and their under-investigational antioxidant, antibacterial, and anticancer, antidiabetic, antifungal and anti-inflammatory properties. This review provides instructions and suggestions for additional studies based on AgNPs. This evaluation also pushes researchers to look into natural resources like plant parts in order to create useful nanobiotechnology.

Antioxidants activities of phytochemicals perspective modulation of autophagy and apoptosis to treating cancer.

The study of chemicals extracted from natural sources should be encouraged due to the significant number of cancer deaths each year and the financial burden imposed by this disease on society. The causes of almost all cancers involve a combination of lifestyle, environmental factors, and genetic and inherited factors. Modern medicine researchers are increasingly interested in traditional phytochemicals as they hold potential for new bioactive compounds with medical applications. Recent publications have provided evidence of the antitumor properties of phytochemicals, a key component of traditional Chinese medicine, thereby opening new avenues for their use in modern medicine. Various studies have demonstrated a strong correlation between apoptosis and autophagy, two critical mechanisms involved in cancer formation and regulation, indicating diverse forms of crosstalk between them. Phytochemicals have the ability to activate both pro-apoptotic and pro-autophagic pathways. Therefore, understanding how phytochemicals influence the relationship between apoptosis and autophagy is crucial for developing a new cancer treatment strategy that targets these molecular mechanisms. This review aims to explore natural phytochemicals that have demonstrated anticancer effects, focusing on their role in regulating the crosstalk between apoptosis and autophagy, which contributes to uncontrolled tumor cell growth. Additionally, the review highlights the limitations and challenges of current research methodologies while suggesting potential avenues for future research in this field.

Assessing stocks of Mystus tengara (Hamilton, 1822) from three different management systems in Baors (Oxbow lake) of southwest Bangladesh: Implications for sustainable management.

This study was conducted to observe the stock assessments of Tengara (Mystus tengara) in three different management systems of Baors (Oxbow lake) such as System-1, System-2, and System-3. In this study, 1806 specimens were sampled using traditional fishing nets to observe growth pattern, population structure, growth parameters, natural mortality (M), fishing mortality (F), total mortality (Z), recruitment pattern, exploitation rate (E), relative yield per-recruit (Y'/R), optimum catchable length, length at first capture, steady state biomass (SSB), and maximum sustainable yield (MSY) from January to December 2021. Digital slide calipers and a digital balance were used to measure each individual's total length (TL) and body weight (BW), respectively. An empirical maximum length-based model was used to calculate size at first sexual maturity (Lm), and optimum catchable length (Lopt) was calculated based on asymptotic length (L∞). The least square linear regression equation was used to determine the regression parameters. The value of regression parameter, 'b' was 3.01 for system-1, 2.78 for system-2, and 2.70 for system-3, indicating that growth pattern of Tengara is isometric in system-1, but negative allometric growth in system-2 and system-3. The highest asymptotic length (L∞) and weight (W∞) of Tengara were found in system-1 (11.19 cm and 13.67 g) in comparison with system-2, (10.98 cm and 12.49 g) and system-3 (9.09 cm and 6.96 g) respectively. The growth coefficient (K) of the von Bertalanffy growth function (VBGF) was 0.72 year-1, 0.72 year-1, and 0.73 year-1 for system-1, system-2 and system-3, respectively. The calculated M, F, Z were 1.72, 1.28, and 3.00 year-1 for system-1, 1.11, 0.67 and 1.78 year-1 for system-2 and 1.12, 0.84 and 1.96 year-1 for system-3 respectively. The calculated life span (tmax) was found 4.19 years for system-1, 4.15 years for system-2 and 4.12 years for system-3. The recruitment patterns showed that the highest relative percentage of recruits were found in July, June and September for system-1, system-2 and system-3 respectively, with the major recruitment peak occurring from April to June for system-1, May to June for system-2 and June to July for system-3. One minor recruitment peak also occurred from August to September in system-1. The exploitation rate was more or less same in all three systems indicating that Tengara is under exploited from all the Baors. The significantly highest SSB and MSY were found in system-1 (22.65 and 12.11 metric tons), compared to system-2 (16.16 and 10.28 metric tons) and system-3 (5.55 and 5.49 metric tons), respectively. Considering the values of regression parameters, recruitment pattern, SSB and MSY, system-1 was found more suitable for Tengara compared to system-2 and system-3 management practices of Baors. Finally, these findings will turn out to be paradigm for the impregnable management of Tengara in Baors of southwest Bangladesh.

Autophagy and Female Fertility: Mechanisms, Clinical Implications, and Emerging Therapies.

Autophagy, an evolutionarily conserved cellular mechanism essential for maintaining internal stability, plays a crucial function in female reproductive ability. In this review, we discuss the complex interplay between autophagy and several facets of female reproductive health, encompassing pregnancy, ovarian functions, gynecologic malignancies, endometriosis, and infertility. Existing research emphasizes the crucial significance of autophagy in embryo implantation, specifically in the endometrium, highlighting its necessity in ensuring proper fetal development. Although some knowledge has been gained, there is still a lack of research on the specific molecular impacts of autophagy on the quality of oocytes, the growth of follicles, and general reproductive health. Autophagy plays a role in the maturation, quality, and development of oocytes. It is also involved in reproductive aging, contributing to reductions in reproductive function that occur with age. This review explores the physiological functions of autophagy in the female reproductive system, its participation in reproductive toxicity, and its important connections with the endometrium and embryo. In addition, this study investigates the possibility of emerging treatment approaches that aim to modify autophagy, using both natural substances and synthetic molecules, to improve female fertility and reproductive outcomes. Additionally, this review intends to inspire future exploration into the intricate role of autophagy in female reproductive health by reviewing recent studies and pinpointing areas where current knowledge is lacking. Subsequent investigations should prioritize the conversion of these discoveries into practical uses in the medical field, which could potentially result in groundbreaking therapies for infertility and other difficulties related to reproduction. Therefore, gaining a comprehensive understanding of the many effects of autophagy on female fertility would not only further the field of reproductive biology but also open new possibilities for diagnostic and treatment methods.

Sulforaphane regulates cell proliferation and induces apoptotic cell death mediated by ROS-cell cycle arrest in pancreatic cancer cells.

Background: Pancreatic cancer (PC), sometimes referred to as pancreatic ductal adenocarcinoma (PDAC), is a major cause of global mortality from cancer. Pancreatic cancer is a very aggressive and devastating kind of cancer, characterized by limited options for therapy and low possibilities of survival. Sulforaphane (SFN), a naturally occurring sulfur-containing compound, is believed to possess anti-inflammatory, anti-obesity, and anti-cancer characteristics. Objective: However, efficient preventative and treatment measures are essential and SFN has been studied for its ability to suppress pancreatic cancer cell proliferation and induce apoptosis. Methods: Here, SFN induced cytotoxicity and apoptosis in PDAC cell lines such as MIA PaCa-2 and PANC-1 cells, as evaluated by cytotoxicity, colony formation, western blot analysis, fluorescence-activated cell sorting (FACS), reactive oxygen species (ROS) detection, caspase-3 activity assay, immunofluorescence assay, and mitochondrial membrane potential assay. Results: In MIA PaCa-2 and PANC-1 cells, SFN inhibited cell survival and proliferation in a dose-dependent manner. The activation of caspase zymogens results in cleaved PARP and cleaved caspase-3, which is associated with an accumulation in the sub G1 phase. Furthermore, SFN increased ROS level and γH2A.X expression while decreasing mitochondrial membrane potential (ΔΨm). Notably, the ROS scavenger N-Acetyl-L-cysteine (NAC) was shown to reverse SFN-induced cytotoxicity and ROS level. Subsequently, SFN-induced cell cycle arrest and apoptosis induction as a Trojan horse to eliminate pancreatic cancer cells via ROS-mediated pathways were used to inhibit pancreatic cancer cells. Conclusion: Collectively, our data demonstrates that SFN-induced cell death follows the apoptosis pathway, making it a viable target for therapeutic interventions against pancreatic cancer.