Mini Reviews in Medicinal Chemistry - Volume 23, Issue 20, 2023

The benefits of honey have been recognized since ancient times for treating numerous diseases. However, in today's modern era, the use of traditional remedies has been rapidly diminishing due to the complexities of modern lifestyles. While antibiotics are commonly used and effective in treating pathogenic infections, their inappropriate use can lead to the development of resistance among microorganisms, resulting in their widespread prevalence. Therefore, new approaches are constantly required to combat drug-resistant microorganisms, and one practical and useful approach is the use of drug combination treatments. Manuka honey, derived from the manuka tree (Leptospermum scoparium) found exclusively in New Zealand, has garnered significant attention for its biological potential, particularly due to its antioxidant and antimicrobial properties. Moreover, when combined with antibiotics, it has demonstrated the ability to enhance their effectiveness. In this review, we delve into the chemical markers of manuka honey that are currently known, as well as detail the impact of manuka honey on the management of infectious diseases up to the present.

Irisin is a thermogenic hormone that leads to causes energy expenditure by increasing brown adipose tissue (BAT). This protein hormone that enables the conversion of white adipose tissue (WAT) to BAT is the irisin protein. This causes energy expenditure during conversion. WAT stores triglycerides and fatty acids and contains very few mitochondria. They also involve in the development of insulin resistance (IR). WAT, which contains a very small amount of mitochondria, contributes to the formation of IR by storing triglycerides and fatty acids. WAT functions as endocrine tissue in the body, synthesizing various molecules such as leptin, ghrelin, NUCB2/nesfatin-1, and irisin along with fat storage. BAT is quite effective in energy expenditure, unlike WAT. The number of mitochondria and lipid droplets composed of multicellular cells in BAT is much higher when compared to WAT. BAT contains a protein called uncoupling protein-1 (UCP1) in the mitochondrial membranes. This protein pumps protons from the intermembrane space toward the mitochondrial matrix. When UCP1 is activated, heat dissipation occurs while ATP synthesis does not occur, because UCP1 is a division protein. At the same time, BAT regulates body temperature in infants. Its effectiveness in adults became clear after the discovery of irisin. The molecular mechanism of exercise, which increases calorie expenditure, became clear with the discovery of irisin. Thus, the isolation of irisin led to the clarification of metabolic events and fat metabolism. In this review, literature information will be given on the effect of irisin hormone on energy metabolism and metabolic syndrome (MetS).

Introduction: Parkinson’s disease (PD) is characterized by fibrillation of disordered proteins known as Lewy bodies in the substantia nigra that also undergo progressive neurodegeneration. The aggregation of α-synuclein (α-syn) is a hallmark and potentially a critical step in the development of Parkinson’s disease and other synucleinopathies. The synaptic vesicle protein α-syn is a small, abundant, highly conserved disordered protein and the causative agent of neurodegenerative diseases. Several novel pharmacologically active compounds are used to treat PD and other neurodegenerative disorders. Though, the mechanism through which these molecules inhibit the α-syn aggregation is still not fully understood. Objective: This review article is focused on the recent advancements in compounds that can inhibit the development of α-syn fibrillation and oligomerization. Methods: The current review article is based on the most recent and frequently cited papers from Google Scholar, SciFinder, and Researchgate sources. Description: In the progression of PD, the mechanism of α-syn aggregation involves the structural transformation from monomers into amyloid fibrils. As the accumulation of α-syn in the brain has been linked to many disorders, the recent search for disease-modifying medications mainly focused on modifying the α-syn aggregation. This review contains a detailed report of literature findings and illustrates the unique structural features, structure-activity relationship, and therapeutic potential of the natural flavonoids in the inhibition of α-syn are also discussed. Conclusion: Recently, many naturally occurring molecules such as curcumin, polyphenols, nicotine, EGCG, and stilbene have been recognized to inhibit the fibrillation and toxicity of α-syn. Therefore, knowing the α-synuclein filament's structure and how they originate will help invent particular biomarkers for synucleinopathies and develop reliable and effective mechanism-based therapeutics. We hope the information this review provides may help evaluate novel chemical compounds, such as α- syn aggregation inhibitors, and will contribute to developing novel drugs for treating Parkinson’s disease.

Polycystic ovary syndrome (PCOS) is a highly widespread disorder caused by a disturbed endocrine system. The Rotterdam criteria have classified 4 phenotypes of PCOS. This syndrome has multifactorial pathophysiology triggered by a disturbed neuroendocrine system, which further produces abnormal levels of luteinizing hormone, follicle-stimulating hormone, androgen, estrogen, and progesterone, leading towards the risk of metabolic and reproductive diseases. PCOS is associated with an increased risk of developing health problems like hyperinsulinemia, diabetes mellitus, hypertension, cardiovascular disorders, dyslipidaemia, endometrial hyperplasia, anxiety and depression. These days, PCOS has become a scientific issue due to complex aetiology with multi- complex physiology. Due to the unavailability of specific medicines, there is no cure for PCOS; however, certain symptoms could be treated. The scientific community is actively looking for various treatment options too. In this context, the current review summarizes the challenges, consequences and various treatment options for PCOS. Various literature reports provide evidence that PCOS can be identified in early infancy, adolescents and women at the menopausal stage. Most commonly, PCOS is caused by multifactorial agents, including genetics and negative lifestyle. Metabolic consequences from obesity, insulin resistance, and vascular disorder have increased the rate of PCOS. This study also highlights psychological morbidity in PCOS women that have an adverse effect on health-related quality of life (HRQoL). PCOS symptoms can be treated using different strategies, including oral contraceptive drugs, surgical treatment (laparoscopic ovarian drilling (LOD), assisted reproductive techniques (ART), and Chinese acupuncture treatment.

Background: Long non-coding RNAs (lncRNAs) are transcripts that are over 200 nucleotides in length and lack protein-coding potential. Despite their name, lncRNAs have important regulatory roles in transcription, translation, and protein function by interacting with DNA, RNA, and protein molecules. Small nucleolar RNAs (snoRNAs), found in various tumors, are encoded by lncRNAs and have gained attention in recent research. The lncRNAs, encoding snoRNAs are known as small nucleolar RNA host genes (SNHGs), a newly identified class of lncRNAs. SNHG11, a specific SNHG, is a critical regulatory factor involved in various biological processes. Accumulating evidence suggests that SNHG11 can impact tumor development and inflammatory diseases by modulating downstream gene expression through chromatin modification, transcription, or post-transcriptional mechanisms. The expression levels of SNHG11 vary significantly in different normal tissues, tumors, and stages of tumor development. Currently, treatment options for advanced cancers are mainly palliative and lack curative potential. Objectives: This review aims to explore the modifications and functions of lncRNA SNHG11 in various tumors and inflammatory diseases. Through a comprehensive analysis of relevant literature on SNHG11 in PubMed, the review aims to provide a comprehensive description of the roles of SNHG11 in known tumors and inflammatory diseases and elucidate the specific mechanism’s underlying functions. The changes in SNHG11 expression in tumors and inflammatory diseases can serve as early biomarkers, therapeutic targets, and prognostic indicators. Improving the clinical detection, staging, treatment, and prognosis of tumors is of great value. Additionally, the structural modifications of SNHG11 can potentially enhance its function as a drug carrier to maximize the therapeutic potential of drugs. Furthermore, understanding the specific mechanisms of SNHG11 in tumors and inflammatory diseases may provide new ways for targeted therapy. Materials and Methods: Relevant studies were retrieved and collected from the PubMed system. SNHG11 was identified as the research object, and research literature on SNHG11 in the past ten years was analyzed to determine its strong association with the onset and progression of various diseases. The precise mechanisms of SNHG11's mode of action were reviewed, and references were further determined based on their impact factors for comprehensive analysis. Results: Through review and analysis, it was found that SNHG11 is involved in a wide range of tumors and inflammatory diseases through its high expression, including lung cancer, colorectal cancer, prostate cancer, hepatocellular carcinoma, triple-negative breast cancer, gastric cancer, glioma, ovarian cancer, pancreatic cancer, acute pancreatitis, and ischemic stroke, but with lower expression in virus myocarditis. SNHG11 is abnormally expressed in cells of these tumors and inflammatory diseases mainly contributes to disease proliferation, metastasis, ceRNA activity, miRNA sponging, drug resistance, and tumor prognosis. However, the specific mechanisms of SNHG11 in tumors and inflammatory diseases require further detailed exploration. Understanding the known regulatory mechanisms can expand the scope of clinical applications and promote early clinical detection, monitoring, and treatment. Conclusion: LncRNA SNHG11 can serve as an early diagnostic biomarker, therapeutic target, and prognostic indicator in various diseases, particularly tumors. SNHG11 plays a crucial role in the occurrence and development of tumors and inflammatory diseases through various mechanisms, which has significant implications for clinical diagnosis and treatment.