Search

Asiatic acid (AA) is a polyphenolic compound with potent antioxidative and anti-inflammatory activities that make it a potential choice to attenuate inflammation and oxidative insults associated with ulcerative colitis (UC). Hence, the present study aimed to evaluate if AA can attenuate molecular, biochemical, and histological alterations in the acetic acid-induced UC model in rats. To perform the study, five groups were applied, including the control, acetic acid-induced UC, UC-treated with 40 mg/kg aminosalicylate (5-ASA), UC-treated with 20 mg/kg AA, and UC-treated with 40 mg/kg AA. Levels of different markers of inflammation, oxidative stress, and apoptosis were studied along with histological approaches. The induction of UC increased the levels of lipid peroxidation (LPO) and nitric oxide (NO). Additionally, the nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream antioxidant proteins [catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH), glutathione peroxidase (GPx), and glutathione reductase (GR)] were down-regulated in the colon tissue. Moreover, the inflammatory mediators [myeloperoxidase (MPO), monocyte chemotactic protein 1 (MCP1), prostaglandin E2 (PGE2), nuclear factor-kappa B (NF-B), tumor necrosis factor-a (TNF-a), and interleukin-1ß (IL-1ß)] were increased in the colon tissue after the induction of UC. Notably, an apoptotic response was developed, as demonstrated by the increased caspase-3 and Bax and decreased Bcl2. Interestingly, AA administration at both doses lessened the molecular, biochemical, and histopathological changes following the induction in the colon tissue of UC. In conclusion, AA could improve the antioxidative status and attenuate the inflammatory and apoptotic challenges associated with UC. [ABSTRACT FROM AUTHOR]

Cancer is a major public health concern worldwide in terms of mortality. The exact reason behind the development of cancer is not understood clearly, but it is evidenced that alcohol consumption, radiation, and exposure to chemicals are main players in this pathogenesis. The current mode of treatments such as surgery, chemotherapy, and radiotherapy are effective, but, still, cancer is a major problem leading to death and other side effects. However, safer and effective treatment modules are needed to overcome the adverse effects of current treatment modules. In this regard, natural compounds have been recognized to ameliorate diseases by exerting anti-inflammatory, anti-oxidative, and anti-tumor potential through several mechanisms. Mangiferin, a xanthone C-glucoside, is found in several plant species including Mangifera indica (mango), and its role in disease prevention has been confirmed through its antioxidant and anti-inflammatory properties. Furthermore, its anti-cancer-potential mechanism has been designated through modulation of cell signaling pathways such as inflammation, angiogenesis, PI3K/AKT, apoptosis, and cell cycle. This article extensively reviews the anticancer potential of mangiferin in different cancers through the modulation of cell signaling pathways. Moreover, the synergistic effects of this compound with some commonly used anti-cancer drugs against different cancer cells are discussed. More clinical trials should be performed to reconnoiter the anti-cancer potential of this compound in human cancer treatment. Further, understanding of mechanisms of action and the safety level of this compound can help to manage diseases, including cancer. [ABSTRACT FROM AUTHOR]

Key Clinical Message: Rhizomelic chondrodysplasia punctata (RCDP) is a rare disorder (~1 in 100,000 live births) of faulty plasmalogen biosynthesis and defective peroxisomal metabolism. RCDP type 2 is specifically caused by glyceronephosphate O‐acyltransferase (GNPAT) gene mutations and is inherited as an autosomal recessive trait. The disorder is characterized by skeletal abnormalities, distinctive facial features, intellectual disability, and respiratory distress. The case report describes a newborn baby with a dysmorphic facial appearance and skeletal abnormalities who was admitted to neonatal intensive care with respiratory distress. His parents were first cousins. The whole exome sequencing for this patient identified an interesting homozygous variant in the GNPAT gene [GNPAT (NM_014236.4):c.1602+1G>A (p.?), Chr1 (GRCh37):g.231408138G>A]. This case report aims to highlight the patient's clinical presentation with the variant and the whole exome sequencing, indicating the identification of a novel mutation in the GNPAT gene causing RCDP type 2. [ABSTRACT FROM AUTHOR]

Exposure to lead (Pb) is associated with serious health problems including hepatorenal toxicity. Apigenin is a natural‐sourced flavonoid with promising antioxidant and anti‐inflammatory effects. In this research, we investigated the potential protective role of apigenin against lead acetate (PbAc)‐induced hepatorenal damage. Thus, this experiment studied the exposure of male Wistar Albino rats to apigenin and/or PbAc and their effects in comparison to the control rats. Apigenin administration decreased the levels of Pb and prevented the histopathological deformations in liver and kidney tissues following PbAc exposure. This was confirmed by the normalized levels of liver and kidney function markers. Additionally, apigenin inhibited significantly oxidative reactions through upregulating Nrf2 and HO‐1, and activating their downstreamed antioxidants accompanied by a marked depletion of pro‐oxidants. Moreover, apigenin decreased the elevated pro‐inflammatory cytokines and inhibited cell loss in liver and kidney tissues in response to PbAc intoxication in both tissues. The obtained results demonstrated that apigenin could be used to attenuate the molecular, biochemical, and histological alterations associated with Pb exposure due to its potent antioxidant, anti‐inflammatory, and antiapoptotic effects. [ABSTRACT FROM AUTHOR]

Blood cancers are characterized by pathological disorders causing uncontrolled hematological cell division. Various strategies were previously explored for the treatment of blood cancers, including chemotherapy, Car-T therapy, targeting chimeric antigen receptors, and platelets therapy. However, all these therapies pose serious challenges that limit their use in blood cancer therapy, such as poor metabolism. Furthermore, the solubility and stability of anticancer drugs limit efficacy and bio-distribution and cause toxicity. The isolation and purification of natural killer cells during Car-T cell therapy is a major challenge. To cope with these challenges, treatment strategies from phyto-medicine scaffolds have been evaluated for blood cancer treatments. Carotenoids represent a versatile class of phytochemical that offer therapeutic efficacy in the treatment of cancer, and specifically blood cancer. Carotenoids, through various signaling pathways and mechanisms, such as the activation of AMPK, expression of autophagy biochemical markers (p62/LC3-II), activation of Keap1-Nrf2/EpRE/ARE signaaling pathway, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), increased level of reactive oxygen species, cleaved poly (ADP-ribose) polymerase (c-PARP), c-caspase-3, -7, decreased level of Bcl-xL, cycle arrest at the G0/G1 phase, and decreasing STAT3 expression results in apoptosis induction and inhibition of cancer cell proliferation. This review article focuses the therapeutic potential of carotenoids in blood cancers, addressing various mechanisms and signaling pathways that mediate their therapeutic efficacy. [ABSTRACT FROM AUTHOR]

The 12th author's name is spelled incorrectly. The correct name is: Abdullah Hamadi.By Osama M. Al-Amer; Atif Abdulwahab A. Oyouni; Mohammed Ali Alshehri; Abdulrahman Alasmari; Othman R. Alzahrani; Saad Ali S. Aljohani; Noura Alasmael; Abdulrahman Theyab; Mohammad Algahtani; Hadeel Al Sadoun; Khalaf F. Alsharif; Abdullah Hamadi; Wed A. Abdali and Yousef MohammedRabaa HawasawiReported by Author; Author; Author; Author; Author; Author; Author; Author; Author; Author; Author; Author; Author; Author [Extracted from the article]

DNA is the hereditary material found in all cells of a human being. The genetic information is passed on through the processes of transcription and translation that result in the formation of proteins. DNA testing is a powerful tool for forensic analysis. DNA can be extracted from any biological material exchanged during a crime scene and analyzed through various techniques. Restriction fragment length polymorphism is one the oldest DNA analysis techniques that produces unique DNA fragment pattern for every individual. However, this technique requires large amount of DNA and was replaced with more efficient methods like polymerase chain reaction that works with even very small amount of sample DNA. New techniques like short tandem repeat analysis have even more discriminating power than simple PCR analysis. Forensic DNA testing has improved a lot over the past few decades and is expected to improve further as the technology is still evolving to provide faster and discriminating results. [ABSTRACT FROM AUTHOR]

Stem cell therapy has emerged as a promising approach for regenerative medicine, offering potential treatments for a wide range of diseases and injuries. Although stem cell therapy has great promise, several obstacles have prevented its broad clinical adoption. The effectiveness of therapy has been inhibited by problems such as ineffective stem cell differentiation, low post-transplantation survival rates, and restricted control over stem cell behavior. Furthermore, the implementation of stem cell therapies is further complicated by the possibility of immunological rejection and cancer. Innovative strategies that provide precise control over stem cell characteristics and maximize their therapeutic potential are desperately needed to overcome these obstacles. Recent studies have shown that the effectiveness of stem cell treatments can be greatly increased by nanoscale advances. By establishing an ideal microenvironment and precisely offering growth factors, nanomaterials such as nanoparticles, nanocomposites, and quantum dots have been demonstrated to improve stem cell differentiation and proliferation. This article provides an overview of the recent trends and applications of nanoscale innovations in the context of stem cell therapy. The recent development of precision medicine has been facilitated by the incorporation of nanotechnology into stem cell therapy. The ability to manipulate stem cells at the nanoscale offers unprecedented control over their behavior and function, opening up exciting possibilities for personalized and highly effective therapeutic interventions. This review paper highlights the recent trends and applications of nanotechnology in advancing stem cell therapy, showcasing its potential to revolutionize regenerative medicine., (Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc.)

Background: Diabetes mellitus (DM) is a chronic metabolic disorder. Hepatopathy is one of the serious effects of DM Melatonin (MT) is a potent endogenous antioxidant that can control insulin output. However, little information is available about the potential association between melatonin and hepatic alpha-fetoprotein expression in diabetes., Objective: This study was conducted to assess the influence of MT on diabetes-related hepatic injuries and to determine how β-cells of the pancreas in diabetic rats respond to MT administration., Materials and Methods: Forty rats were assigned to four groups at random (ten animals per group). Group I served as a normal control group. Group II was induced with DM, and a single dose of freshly prepared streptozotocin (45 mg/kg body weight) was intraperitoneally injected. In Group III, rats received 10 mg/kg/day of intraperitoneal melatonin (IP MT) intraperitoneally over a period of 4 weeks. In Group IV (DM + MT), following the induction of diabetes, rats received MT (the same as in Group III). Fasting blood sugar, glycosylated hemoglobin (HbA1c), and serum insulin levels were assessed at the end of the experimental period. Serum liver function tests were performed. The pancreas and liver were examined histopathologically and immunohistochemically for insulin and alpha-fetoprotein (AFP) antibodies, respectively., Results: MT was found to significantly modulate the raised blood glucose, HbA1c, and insulin levels induced by diabetes, as well as the decreased alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Furthermore, MT attenuated diabetic degenerative changes in the pancreas and the hepatic histological structure, increased the β-cell percentage area, and decreased AFP expression in the liver tissue. It attenuated diabetes-induced hepatic injury by restoring pancreatic β-cells; its antioxidant effect also reduced hepatocyte injury., Conclusion: Collectively, the present study confirmed the potential benefits of MT in downregulating the increased hepatic alpha-fetoprotein expression and in restoring pancreatic β-cells in a streptozotocin-induced diabetic rat model, suggesting its promising role in the treatment of diabetes., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Alsharif, Hamad, Alblihd, Ali, Mohammed, Theyab, Al-Amer, Almuqati, Almalki, Albarakati, Alzahrani, Albrakati, Albarakati, Abass, Lokman and Elmahallawy.)