Neuroprotective effects of brown rice consumption in an iron-induced parkinsonism in Drosophila.

OBJECTIVES: Iron (Fe) accumulation and resultant oxidative stress play a significant role in the neuronal death observed in Parkinson's disease (PD). Brown rice (BR) possesses antioxidant properties able to reduce cellular oxidative damage. Thus, we hypothesized that BR may ameliorate Fe-induced parkinsonism due to oxidative stress. METHODS: Two - to three-day-old male flies were concurrently exposed to Fe (ferrous sulphate, 1 mM) and interventions, divided into eight groups: control; Fe; BR; white rice (WR); L-dopa (1 mM); Fe (1 mM) + BR; Fe (1 mM) + WR; and Fe (1 mM) + L-dopa (1 mM). The flies were exposed for 15 days to their respective diets, and their behavior, relevant biomarkers, and the expression of related genes were evaluated. RESULTS: Chronic exposure to Fe caused cognitive and locomotor deficits by increasing Fe levels (p = 0.027) in flies' heads, as well as heightened aggression and grooming episodes (p < 0.001). The elevated iron levels induced changes consistent with oxidative stress, evidenced by increased MDA levels (p < 0.001), and reduced activity of catalase (p < 0.001) and glutathione peroxidase (GPx) (p < 0.001), along with decreased dopamine levels (p < 0.001). Additionally, there was dysregulation in the mRNA expression of malvolio, ferritin, Nrf2, DJ-1, GPx, and catalase (p < 0.05). BR prevented the Fe-induced effects (Fe + BR group) even more effectively than L-Dopa (p < 0.001). CONCLUSION: The findings indicate that BR has the potential to mitigate Fe-induced ROS-mediated damage in a Drosophila model of PD-like disease by modulating key players in the Nrf2 signaling pathway.

Age and sex-based impacts of maternal iron deficiency on offspring's cognitive function and anemia: A systematic review.

Iron deficiency is a recognized global health concern, particularly impactful during pregnancy where the mother serves as the primary source of iron for the developing fetus. Adequate maternal iron levels are crucial for fetal growth and cognitive development. This review investigates the correlation between maternal iron deficiency and cognitive impairment and anemia in offspring, considering age and gender differentials. PubMed, ScienceDirect, and Google Scholar databases were queried using keywords "maternal," "iron," "gender/sex," and "cognition." The review included studies on human and animal subjects where maternal iron deficiency was the exposure and offspring cognitive function and anemia were outcomes. Out of 1139 articles screened, fourteen met inclusion criteria. Twelve studies highlighted cognitive deficits in offspring of iron-deficient mothers, with females generally exhibiting milder impairment compared to males. Additionally, two studies noted increased anemia prevalence in offspring of iron-deficient mothers, particularly affecting males and younger individuals. The findings suggest that male offspring are at higher risk of both anemia and cognitive dysfunction during youth, while females face increased risks in adulthood. Thus, maternal iron deficiency elevates the likelihood of anemia and cognitive impairments in offspring, underscoring the importance of addressing maternal iron status for optimal child health.

Iron chelation and supplementation: A comparison in the management of inflammatory bowel disease using drosophila.

AIMS: Inflammatory Bowel Disease (IBD) is associated with systemic iron deficiency and has been managed with iron supplements which cause adverse side effects. Conversely, some reports highlight iron depletion to ameliorate IBD. The underlying intestinal response and comparative benefit of iron depletion and supplementation in IBD is unknown. The aims of this work were to characterize and compare the effects of iron supplementation and iron depletion in IBD. MAIN METHODS: IBD was induced in Drosophila melanogaster using 3 % dextran sodium sulfate (DSS) in diet for 7 days. Using this model, we investigated the impacts of acute iron depletion (using bathophenanthroline disulfonate, BPS) and supplementation (using ferrous sulphate, FS), before and after IBD induction, on gut iron homeostasis, cell death, gut permeability, inflammation, antioxidant defence, antimicrobial response and several fly phenotypes. KEY FINDINGS: DSS decreased fly mass (p < 0.001), increased gut permeability (p < 0.001) and shortened lifespan (p = 0.035) compared to control. The DSS-fed flies also showed significantly elevated lipid peroxidation (p < 0.001), and the upregulated expression of apoptotic marker- drice (p < 0.001), tight junction protein - bbg (p < 0.001), antimicrobial peptide - dpta (p = 0.002) and proinflammatory cytokine - upd2 (p < 0.001). BPS significantly (p < 0.05) increased fly mass and lifespan, decreased gut permeability, decreased lipid peroxidation and decreased levels of drice, bbg, dpta and upd2 in IBD flies. This iron chelation (using BPS) showed better protection from DSS-induced IBD than iron supplementation (using FS). Preventive and curative interventions, by BPS or FS, also differed in outcomes. SIGNIFICANCE: This may inform precise management strategies aimed at tackling IBD and its recurrence.

Neonatal administration of fenofibrate had no developmental programming effect on the lipid profile and relative leucocyte telomere lengths of adolescent rats fed a high-fructose diet postnatally.

Telomere length, a marker of ageing, is susceptible to developmental programming that may cause its accelerated attrition. Metabolic syndrome triggers telomere attrition. Fenofibrate, a peroxisome proliferator-activated receptor-alpha agonist, is protective against telomere attrition. We investigated the impact of fenofibrate administered during suckling on the lipid profile and leucocyte telomere lengths of rats fed a high-fructose diet post-weaning. Suckling Sprague-Dawley pups (n = 119) were allocated to four groups and gavaged with either 10 mL·kg-1 body mass 0.5% dimethyl sulfoxide, 100 mg·kg-1 body mass fenofibrate, fructose (20%, w / v), or a combination of fenofibrate and fructose for 15 days. Upon weaning, each of the initial groups was split into two subgroups: one had plain water while the other had fructose solution (20%, w / v) to drink for 6 weeks. Blood was collected for DNA extraction and relative leucocyte telomere length determination by real-time PCR. Plasma triglycerides and cholesterol were also quantified. The treatments had no effect (p > 0.05) on body mass, cholesterol concentration, and relative leucocyte telomere lengths in both sexes. Post-weaning fructose increased triglyceride concentrations (p < 0.05) in female rats. Fenofibrate administered during suckling did not affect ageing nor did it prevent high fructose-induced hypertriglyceridaemia in female rats.

LncRNA SNHG15: A potential therapeutic target in the treatment of colorectal cancer.

The global burden of colorectal cancer (CRC) is increasing annually. CRC could develop from genetic and phenotypic factors involving changes in gene expression. Incredibly, the human genome transcribes into non-coding RNAs, among which long non-coding RNAs (lncRNAs) signify the most crucial part of the transcriptome in multicellular organisms. lncRNAs affect gene expression at multiple levels, from transcription to protein localization and stability. Recent studies have implicated lncRNA small nucleolar RNA host gene 15 (SNHG15) in cancers occurrence and progression. Previously, an indication suggests SNHG15 overexpression triggers proliferation, metastasis, and impedes apoptosis in CRC. Further, through its activity of binding micro-RNAs, lncRNA SNHG15 modulates genes associated with CRC progression and promotes CRC resistance to chemotherapeutic drugs. Here, we reviewed recent findings on the various mechanisms and roles of lncRNA SNHG15 implicated in CRC tumorigenesis. We further highlight how SNHG15 plays a vital role in regulating critical pathways linked to the development and progression of CRC. Finally, we highlight how SNHG15 can be modulated for CRC treatments and the various therapeutic strategies to be implored when targeting SNHG15 in the context of CRC treatments. Findings from these studies present SNHG15 as a potential therapeutic target for preventing and treating CRC.

Hepatitis B Therapeutic Vaccine: A Patent Review.

Viral hepatitis has long been underrated as a danger to global health. The UN only recently called for worldwide action to tackle viral hepatitis and lessen the disease burden in its "2030 Agenda for Sustainable Development". Hepatitis B virus (HBV), which causes liver cirrhosis and malignancy, is a main cause of death globally. This review analyses innovative HBV therapeutic vaccine candidates for which a patent was filed between January 2010 and March 2022 and presents future improvement techniques for vaccine efficacy. Although there is a preventative vaccine for HBV infection, over 3% of people worldwide have the disease on a long-term basis and can no longer benefit from it. Most people will have chronic HBV infection for the rest of their lives once it has been diagnosed. Moreover, only a small percentage of treated patients experience a functional cure with persistent hepatitis B surface antigen reduction. A significant proportion of deaths are caused by liver cirrhosis and hepatocellular cancer, which are both caused by chronic hepatitis B infection. Hence, there is an urgent need for novel medications due to the inadequacies of the current therapies.

MALAT1: A Promising Therapeutic Target for the Treatment of Metastatic Colorectal Cancer.

Cancer metastasis research has emerged in recent years as one of the most important topics of debate in the discovery and development of novel anticancer therapies. Colorectal cancer (CRC), the third most common cancer worldwide, has a high mortality rate due to recurrence and distant metastasis to the liver. Several non-coding RNAs (ncRNAs) have been linked to metastatic CRC (mCRC), including the long non-coding RNA (lncRNA) Metastasis-Associated Lung-Adenocarcinoma Transcript 1 (MALAT1). MALAT1 is an RNA that has been linked to tumor cell proliferation, progression, epithelial-mesenchymal transition (EMT), cell migration and invasion, metastasis, and survival in mammalian species. Previously, there was no convincing evidence linking MALAT1 to mCRC. Studies have shown that MALAT1 functions as a competitive endogenous RNA (ceRNA) with microRNAs (miRNAs) and interacts directly with oncogenes and proteins. This RNA also activates several signaling pathways, including Wnt/ß-catenin, PI3K/Akt/mTOR, and EMT. Meanwhile, standard chemotherapy and immunotherapy are the current treatment options for mCRC patients. However, evidence-based studies have recently demonstrated that inhibiting the MALAT1 RNA transcript can be considered as a treatment option for mCRC, highlighting the need to investigate its roles as a therapeutic target in mCRC. Thus, in this review, we looked at studies that linked MALAT1 to multiple signaling pathways implicated in mCRC, as well as its potential as a therapeutic target for the treatment of mCRC.