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Oxidative stress involved in various pathological conditions. Plants have been proven to act as a natural exogenous antioxidant. The aim of this research is to investigate the protective effects of Etlingera coccinea leaves aqueous extract on autoxidation-induced ox brain homogenate. The brain homogenate was divided into 7 groups: control group with PBS solution, positive control group with 100 μg/ml ascorbic acid, test group with 25, 50, 100, 200 and 400 μg/ml of E. coccinea. The antioxidant potential of E. coccinea aqueous extract has been evaluated by antioxidant capacity assay such as Total phenolic content (TPC), radical scavenging assay (DPPH) and ferric reducing antioxidant power (FRAP). Malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) were also measured at 0 hr and 1 hr after 37°C water bath incubation to determine the antioxidant status and oxidative damage. TPC assay showed (4.85 ± 0.28) mg GAE/g of dry weight of E. coccinea leaves. Based on DPPH and FRAP assay, E. coccinea aqueous extract showed a dose-dependent antioxidant activity. MDA level in the 50 μg/ml E. coccinea was significantly lower compared to the other groups (p < 0.05). The SOD activity was significantly increase in 400 μg/ml E. coccinea (p < 0.05) compared to other groups. E. coccinea at the dose of 25 μg/ml and 50 μg/ml showed significant increase in GSH level compared to other groups (p < 0.05). In conclusion, 25 μg/ml and 50 μg/ml of E. coccinea leave aqueous extracts exhibited a potential protective effect on autoxidation-induced ox brain homogenate. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases (CVD) are the number one cause of death worldwide, with atherosclerosis, which is the formation of fatty plaques in the arteries, being the most common underlying cause. The activation of inflammatory events and endothelium dysfunction are crucial for the development and pathophysiology of atherosclerosis. Elevated circulating levels of low-density lipoprotein (LDL) have been associated with severity of atherosclerosis. LDL can undergo oxidative modifications, resulting in oxidised LDL (oxLDL). OxLDL has been found to have antigenic potential and contribute significantly to atherosclerosis-associated inflammation by activating innate and adaptive immunity. Various inflammatory stimuli such as interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-α) and intercellular adhesion molecule 1 (ICAM-1) play major roles in atherosclerosis. To date, studies have provided valuable insights into the role of oxLDL in the development of atherosclerosis. However, there remains a gap in understanding the specific pathways involved in this process. This review aims to provide and discuss the mechanisms by which oxLDL modulates signalling pathways that cause cardiovascular diseases by providing in vitro and in vivo experimental evidence. Its critical role in triggering and sustaining endothelial dysfunction highlights its potential as a therapeutic target. Advancing the understanding of its atherogenic role and associated signalling pathways could pave the way for novel targeted therapeutic strategies to combat atherosclerosis more effectively. [ABSTRACT FROM AUTHOR]

Overactivation of the angiotensin-converting enzyme (ACE)/angiotensin II type 1 receptor (AT1R) pathway leads to vasoconstriction and elevated blood pressure. Persicaria minor (Huds.) Opiz is an herbal plant known for its antioxidant, anti-hyperlipidemic, and anti-atherosclerotic properties, with bioactive compounds that exhibit antihypertensive effects. Therefore, this study aimed to evaluate the antihypertensive effects of the standardized aqueous extract of P. minor leaf (AEPM) through the ACE/AT1R pathway in human umbilical vein endothelial cells (HUVECs) induced with phorbol 12-myristate 13-acetate (PMA). HUVECs were stimulated with PMA to induce ACE, with or without AEPM or captopril treatment, for 24 h. Subsequently, ACE mRNA expression, ACE protein levels, ACE activity, angiotensin II levels, and AT1R expression were measured. The results demonstrated that AEPM treatment significantly reduced ACE mRNA expression, ACE protein levels, ACE activity, angiotensin II levels, and AT1R expression in PMA-induced HUVECs. The modulatory effects of AEPM on the ACE/AT1R pathway were comparable to those of captopril. Ex vivo experiments further confirmed that AEPM reduced the contraction responses of rat aortic rings to PMA. In conclusion, P. minor effectively inhibits the ACE/AT1R pathway in PMA-induced HUVECs, suggesting its potential as a natural antihypertensive agent. [ABSTRACT FROM AUTHOR]

Background and Objectives: Enterococcus faecalis is known as common pathogen for endodontic infections and cause secondary and refractory pulp periapical periodontitis. The bacteria can opportunistically colonize periodontal pockets and presents a possibility of infection developing in other organs. This research will investigate the dissemination of E. faecalis from the gingival tissue to the heart and kidney. Materials and Methods: Three groups were formed, consisting of twelve male Sprague Dawley rats: a control group designated as 0-day, and experimental groups labeled as 7-days and 14-days. Periodontitis induced by concurrent infection with sterile wire 0.2 mm insertion and E. faecalis inoculation is performed into the gingival sulcus located between the maxillary right 1st and 2nd molar teeth area. After euthanasia, tissue samples around the maxillary gingiva, maxillary jaw samples, kidney and heart tissues were obtained for quantitative Real-Time PCR assay and histopathological analysis. Results: Results showed at 7-days, there was an upregulation of E. faecalis gene expression in the gingiva, heart, and kidney samples as well as infiltration of the inflammatory cells at 7-days post induction, which consequently decreased at 14-days. Conclusion: Thus, the study suggests dissemination of E. faecalis from gingival tissue to the heart, kidney which could be probable link between periodontal disease, heart, and kidney disease. [ABSTRACT FROM AUTHOR]

Organotin (IV) dithiocarbamate has recently received attention as a therapeutic agent among organotin (IV) compounds. The individual properties of the organotin (IV) and dithiocarbamate moieties in the hybrid complex form a synergy of action that stimulates increased biological activity. Organotin (IV) components have been shown to play a crucial role in cytotoxicity. The biological effects of organotin compounds are believed to be influenced by the number of Sn-C bonds and the number and nature of alkyl or aryl substituents within the organotin structure. Ligands target and react with molecules while preventing unwanted changes in the biomolecules. Organotin (IV) dithiocarbamate compounds have also been shown to have a broad range of cellular, biochemical, and molecular effects, with their toxicity largely determined by their structure. Continuing the investigation of the cytotoxicity of organotin (IV) dithiocarbamates, this mini-review delves into the appropriate method for synthesis and discusses the elemental and spectroscopic analyses and potential cytotoxic effects of these compounds from articles published since 2010. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases (CVDs) represent a broad spectrum of diseases afflicting the heart and blood vessels and remain a major cause of death and disability worldwide. CVD progression is strongly associated with risk factors, including hypertension, hyperglycemia, dyslipidemia, oxidative stress, inflammation, fibrosis, and apoptosis. These risk factors lead to oxidative damage that results in various cardiovascular complications including endothelial dysfunctions, alterations in vascular integrity, the formation of atherosclerosis, as well as incorrigible cardiac remodeling. The use of conventional pharmacological therapy is one of the current preventive measures to control the development of CVDs. However, as undesirable side effects from drug use have become a recent issue, alternative treatment from natural products is being sought in medicinal plants and is gaining interest. Roselle (Hibiscus sabdariffa Linn.) has been reported to contain various bioactive compounds that exert anti-hyperlipidemia, anti-hyperglycemia, anti-hypertension, antioxidative, anti-inflammation, and anti-fibrosis effects. These properties of roselle, especially from its calyx, have relevance to its therapeutic and cardiovascular protection effects in humans. This review summarizes the findings of recent preclinical and clinical studies on roselle as a prophylactic and therapeutic agent in attenuating cardiovascular risk factors and associated mechanisms. [ABSTRACT FROM AUTHOR]

C26H38N2S4Sn, triclinic, P 1 ‾ (no. 2), a = 9.6272(1) Å, b = 12.1043(2) Å, c = 13.3584(2) Å, α = 82.296(1)°, β = 86.611(1)°, γ = 66.912(1)°, V = 1419.02(4) Å3, Z = 2, Rgt(F) = 0.0235, wRref(F2) = 0.0612, T = 100 K. [ABSTRACT FROM AUTHOR]

Cardiovascular disease is the most common cause of death among diabetic patients worldwide. Hence, cardiovascular wellbeing in diabetic patients requires utmost importance in disease management. Recent studies have demonstrated that protein kinase C activation plays a vital role in the development of cardiovascular complications via its activation of mitogen-activated protein kinase (MAPK) cascades, also known as PKC-MAPK pathways. In fact, persistent hyperglycaemia in diabetic conditions contribute to preserved PKC activation mediated by excessive production of diacylglycerol (DAG) and oxidative stress. PKC-MAPK pathways are involved in several cellular responses, including enhancing oxidative stress and activating signalling pathways that lead to uncontrolled cardiac and vascular remodelling and their subsequent dysfunction. In this review, we discuss the recent discovery on the role of PKC-MAPK pathways, the mechanisms involved in the development and progression of diabetic cardiovascular complications, and their potential as therapeutic targets for cardiovascular management in diabetic patients. [ABSTRACT FROM AUTHOR]

Combination therapy emerges as a fundamental scheme in cancer. Many targeted therapeutic agents are developed to be used with chemotherapy or radiation therapy to enhance drug efficacy and reduce toxicity effects. ABT-263, known as navitoclax, mimics the BH3-only proteins of the BCL-2 family and has a high affinity towards pro-survival BCL-2 family proteins (i.e., BCL-XL, BCL-2, BCL-W) to induce cell apoptosis effectively. A single navitoclax action potently ameliorates several tumor progressions, including blood and bone marrow cancer, as well as small cell lung carcinoma. Not only that, but navitoclax alone also therapeutically affects fibrotic disease. Nevertheless, outcomes from the clinical trial of a single navitoclax agent in patients with advanced and relapsed small cell lung cancer demonstrated a limited anti-cancer activity. This brings accumulating evidence of navitoclax to be used concomitantly with other chemotherapeutic agents in several solid and non-solid tumors that are therapeutically benefiting from navitoclax treatment in preclinical studies. Initially, we justify the anti-cancer role of navitoclax in combination therapy. Then, we evaluate the current evidence of navitoclax in combination with the chemotherapeutic agents comprehensively to indicate the primary regulator of this combination strategy in order to produce a therapeutic effect. [ABSTRACT FROM AUTHOR]