Boydmonahan8437
In several in vitro and in vivo models, P. check details ginseng showed potential beneficial effects in lung cancer and inflammation treatment. In this review discussion, we summarized in detail the up-to-date research evidence for anti-lung cancer and anti-inflammatory protective effects of ginsenosides and their potential molecular mechanisms.
In several in vitro and in vivo models, P. ginseng showed potential beneficial effects in lung cancer and inflammation treatment. In this review discussion, we summarized in detail the up-to-date research evidence for anti-lung cancer and anti-inflammatory protective effects of ginsenosides and their potential molecular mechanisms.
Hepatocellular carcinoma (HCC) is one of the most common cancers associated with a high rate of mortality. Disturbance between cell proliferation and cell death is one of the cancer hallmarks. Cell proliferation is mainly controlled by the cell cycle. The arrest of the cell cycle is one of the important targets of anticancer agents exert their therapeutic efficacy.
The present study tries to clarify the exact role of some natural products such as daidzein (DAZ) and alcoholic chicory leaf extract (CE), as possible regulators of cell cycle and apoptosis.
HCC in rats was induced using diethylnitrosamine (DENA). Ninety rats were allocated and divided equally into nine groups, treated with CE, DAZ, a combination of both, and sorafenib, with nontreated control groups.
Treatment with CE, DAZ, and their combination significantly downregulated hepatic tissue expression of cyclin D1/CDK4 axis as well as cyclin A/CDK2 axis. The suggested therapeutic protocol inhibited the proliferation and dampened Bcl-2 expression. Additionally, the combination of CE and DAZ showed a comparable potency to sorafenib in respect to the cyclin D/CDK4 axis, as well as; this protocol was a more potent inhibitor of cyclin A and Ki-67 expression.
Treatment with DAZ or CE alone, or their combination, could possess an inhibitory effect on hepatocarcinogenesis via cell cycle arrest, inhibition of proliferation through suppression of Ki-67 expression, and apoptosis induction, mediated by downregulation of Bcl-2.
Treatment with DAZ or CE alone, or their combination, could possess an inhibitory effect on hepatocarcinogenesis via cell cycle arrest, inhibition of proliferation through suppression of Ki-67 expression, and apoptosis induction, mediated by downregulation of Bcl-2.
Angiogenesis is a hallmark of cancer, which is regulated by diverse factors, including long non-coding RNAs (lncRNAS). Our previous study showed that the long non-coding RNA H22954 inhibits tumor growth, albeit whether it is involved in the angiogenesis of cancer re-mains unknown.
This study aimed to investigate the role of lncRNA H22954 in angiogenesis of acute myeloid leukemia (AML) and the underlying molecular mechanism.
Bioinformatics analysis was conducted to screen the targeted molecule of H22954. Western blot and ELISA analysis detected PDGFA protein expression, and RT-qPCR detected H22954 and PDGFA expression in cell lines and AML samples. Dual-luciferase reporter gene assay and half-life assay were applied to validate the relationship between H22954 and PDGFA. The functional experi-ment was conducted to investigate the role of H22954 in tube formation.
Overexpression of H22954 inhibited angiogenesis in mouse xenograft tumors and cultured acute myeloid leukemia (AML) cells. Bioinformatics analysis and luciferase assay revealed that H22954 targeted the 3' untranslated region (UTR) of the platelet-derived growth factor subunit A (PDGFA) gene. In transfected cells, H22954 overexpression reduced PDGFA expression and protein levels. Tube formation was rescued following the addition of exogenous human PDGFA to the con-ditioned medium from cells overexpressing H22954. The expression of H22954 in K562 cells re-duced the half-life of PDGFA mRNA. Furthermore, H22954 expression was inversely correlated with PDGFA expression in patient samples.
These findings indicate that H22954 inhibits angiogenesis in AML through the down-regulation of PDGFA expression. Administering recombinant lncRNA H22954 may be a therapeutic approach for patients with AML.
These findings indicate that H22954 inhibits angiogenesis in AML through the down-regulation of PDGFA expression. Administering recombinant lncRNA H22954 may be a therapeutic approach for patients with AML.Even today, cancer is one of the prominent leading causes of death worldwide. However, there are a couple of treatment options available for management, but the adverse effects are more prominent compared to therapeutic effects. Therefore, there is a need to design some midway that may help to bypass the negative effects or lower their severity. Using nanotechnology has addressed many issues, even still many miles needed to cover before reaching the center stage. The nanoformulations thus developed can target distant organs owing to their multifunctionality and targeting potential. Stimuli-responsive nanomedicine is one of the most exploited formulations. They can encapsulate and release the drugs for a higher period. However, they release a burst mechanism. The other nano-formulations contain dendrimers, micelles, and lipid-based nano-formulations that have been developed and evaluated for their efficacy in cancer treatment. This review paper highlights some significant patents granted/applied in various patent offices around the globe to treat cancer using nanotechnology. The Google patent, United States Patent and Trademark Office (USPTO), Escapenet, and many others were used as the search engine for patent search, and data were collected and evaluated. They used these patented technologies for diagnostic and treatment options, enhancing the absorption, distribution, metabolism, and excretion (ADME) profile of therapeutic molecules.The gut microbiota is one of the great innovations of modern medicine. In the modern microbiota revolution era, more comprehensive and in-depth studies have been performed as regards the microbial gut communities and their impact on acute and chronic diseases, including those of the nervous system as acute neurological diseases. The microbiota has changed our knowledge of medical conditions; in particular, considering stroke (both ischemic and hemorrhagic), literature studies, experimental and clinical researches indicate that the individual's risk and outcomes are substantially impacted by the gut microbiota. The aim of our review article is to investigate and discuss the recent insights in the emerging role of this complex "gut microbiota-brain axis" in affecting some acute neurological diseases, such as stroke, responsible for a significant number of deaths worldwide. We performed electronic research on PubMed® and collected articles published in the last ten years, finding that changes in the gut microbiota composition could affect various aspects of stroke pathophysiology and individual predisposition, risk and outcomes. Our review article suggests that there is a strong connection between the gut microbiota and the brain, both in health and in acute neurological diseases such as stroke. Investigating and exploring this relationship can be a challenge useful to learn more about this disabling/deadly condition, and it can be a useful tool to identify novel potential therapeutic approaches, improving an individual's outcomes and life.
Type 2 diabetes is a metabolic disease characterized by hyperglycemia on the background of insulin resistance and decreased insulin secretion. A relatively large number of patients with this type of diabetes have abdominal obesity, which also affects insulin resistance development. Chronic hyperglycemia can lead to damage and dysfunction of various organs, and a striking example is diabetic nephropathy. Diabetic nephropathy is a specific kidney damage that occurs due to complications of diabetes and is accompanied by the formation of diffuse or nodular glomerulosclerosis, which can lead to terminal renal failure and requires the immediate substitution of renal therapy or renal transplantation. Diabetic nephropathy is diagnosed with albuminuria and a decrease in the rate of glomerular filtration.
This review was based on a literature search for the most important evidence on the issue of considering vitamin D as a possible method of prevention of obesity, type 2 diabetes, and diabetic nephropathy. Collected published articles were summarized according to their overall themes.
In this review, we considered vitamin D as a possible method of treatment of type 2 diabetes, as well as its complications - diabetic nephropathy.
Studies show that vitamin D inhibits the renin-angiotensin-aldosterone system, resulting in improved renal function in diabetic nephropathy. Vitamin D also has the anti-inflammatory, antiproliferative, and anti-metastatic effect, which improves endothelial function.
Studies show that vitamin D inhibits the renin-angiotensin-aldosterone system, resulting in improved renal function in diabetic nephropathy. Vitamin D also has the anti-inflammatory, antiproliferative, and anti-metastatic effect, which improves endothelial function.
The incidence of cancer has been increasing worldwide. Unfortunately, the drugs used in cancer chemotherapy are toxic to both neoplasms and normal tissues, while many available medications have low potencies. Conjugated α,β-unsaturated ketones differ structurally from contemporary anticancer medications , some of which have noteworthy antineoplastic properties.
This study aimed to design and synthesize highly potent cytotoxins with far greater toxicity to neoplasms than to non-malignant cells.
A series of N-acyl-3,5-bis(benzylidene)-4-piperidone hydrochlorides 4a-n were prepared and evaluated against Ca9-22, HSC-2, HSC-3, and HSC-4 squamous cell carcinomas as well as against HGF, HPLF, and HPC non-malignant cells. QSAR and western blot analyses were performed.
The majority of compounds display submicromolar CC
values towards the neoplasms; the figures for some of the compounds are below 10
M. In general, 4a-n have much lower CC
values than those of melphalan, 5-fluorouracil, and methotrexate, while some compounds are equitoxic with doxorubicin. The compounds are far less toxic to the non-malignant cells, giving rise to substantial selectivity index (SI) figures. A QSAR study revealed that both potency and the SI data were controlled to a large extent by the electronic properties of the substituents in the arylidene aryl rings. Two representative compounds, 4f and 4g, caused apoptosis in HSC-2 cells.
The compounds in series 4 are potent cytotoxins displaying tumor-selective toxicity. In particular, 4g with an average CC
value of 0.04 μM towards four malignant cell lines and a selectivity index of 46.3 is clearly a lead molecule that should be further evaluated.
The compounds in series 4 are potent cytotoxins displaying tumor-selective toxicity. In particular, 4g with an average CC50 value of 0.04 μM towards four malignant cell lines and a selectivity index of 46.3 is clearly a lead molecule that should be further evaluated.
Anatomical imaging methods and histological examinations have limited clinical value for early monitoring of brain function damage after cardiac arrest (CA) in vivo.
We aimed to assess the cerebral protective effects of hydrogen in rabbits with CA by using fluorodeoxyglucose-positron emission tomography/computed tomography (FDG-PET/CT).
Male rabbits were divided into the hydrogen-treated (n=6), control (n=6), and sham (n=3) groups. Maximum standardized uptake values (SUVmax) were measured by FDG-PET/CT at baseline and post-resuscitation. Blood Ubiquitin C-terminal hydrolase-L1 (UCH-L1) and neuron-specific enolase (NSE) were measured before and after the operation. After surgical euthanasia, brain tissues were extracted for Nissl staining.
SUVmax values first decreased at 2 and 24 h after resuscitation before rising in the hydrogentreated and control groups. SUVmax values in the frontal, occipital, and left temporal lobes and in the whole brain were significantly different between the hydrogen and control groups at 2 and 24 h postresuscitation (P<0.
