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1.
Cureus ; 16(5): e60699, 2024 May.
Article in English | MEDLINE | ID: mdl-38910609

ABSTRACT

The utilization of herbal formulations for the management of reproductive tract disorders has been a longstanding practice in traditional medicine. In this study, we investigated the efficacy of a herbal extract, Shalmali (Bombax ceiba), in addressing uterine bleeding, a common concern in gynecological health. Through gene expression analysis, this study examined the impact of Shalmali extract on key genes associated with uterine bleeding, namely ESR1, CD56, and SDF-1, in the human endometrial stromal cell line (T HESC). Our findings revealed a dose-dependent decrease in ESR1 and CD56 gene expression levels following treatment with Shalmali extract, suggesting its potential to modulate hormonal and cellular processes involved in uterine bleeding. Notably, an increase in SDF-1 gene expression was observed, indicating a possible role of Shalmali extract in promoting tissue repair and regeneration. Comparison with the standard drug tranexamic acid demonstrated similar effects on gene expression levels, further validating the therapeutic potential of Shalmali extract. Agarose gel electrophoresis images supported these findings, showing reduced gene expression in cells treated with Shalmali extract comparable to those treated with tranexamic acid. These results underscore the promising efficacy of Shalmali extract as a natural alternative for managing uterine bleeding, potentially offering a safe and effective treatment option for individuals seeking traditional remedies for gynecological concerns. Further research is warranted to elucidate the underlying mechanisms of action and assess the long-term safety and efficacy of Shalmali extract in clinical settings.

2.
J Clin Lab Anal ; 36(5): e24390, 2022 May.
Article in English | MEDLINE | ID: mdl-35388548

ABSTRACT

BACKGROUND: An aberrant expression of long non-coding RNA PVT1 has been associated with apoptosis in various cancer types. We aimed to explore the PVT1 and four apoptosis-related proteins (p53, Bcl2, and PD-1/PD-L1) signature in thyroid cancer (TC). METHODS: The PVT1 expression level was measured in 64 FFPE TC paired samples by real-time quantitative PCR. Overall and stratified analyses by different clinicopathological features were done. The apoptotic proteins were evaluated by immunohistochemistry staining. RESULTS: Overall analysis showed significant PVT1upregulation in TC tissues (p < 0.001). Similarly, subgroup analysis by BRAFV600E mutation showed consistent results. Lower expression of p53 was associated with mortality (p = 0.001). Bcl2 overexpression was associated with greater tumor size (p = 0.005). At the same time, HCV-positive cases were associated with repressed Bcl2 expression levels (54.3% in HCV-negative vs. 6.9% in HCV-positive cases, p = 0.011). PD-1 expression was associated with lymph node metastasis (p = 0.004). Enhanced PD-L1 expression in the tumor was associated with a higher tumor stage, lymphovascular invasion, and mortality risk. Kaplan-Meier curves for overall survival showed that low p53 and high PD-L1 expressions were associated with lower survival time. The p53-positive staining is associated with a 90% decreased mortality risk (HR = 0.10, 95%CI = 0.02-0.47, p = 0.001), while patients with high PD-L1 were five times more likely to die (HR = 4.74, 95%CI = 1.2-18.7, p = 0.027). CONCLUSION: Our results confirm the upregulation of PVT1 in TC. The apoptosis-related proteins (p53, Bcl2, and PD-1/PD-L1) showed different prognostic utility in TC patients; in particular, low p53 and high PD-L1 expressions associated with low survival times. Further large-scale and mechanistic studies are warranted.


Subject(s)
Hepatitis C , Thyroid Neoplasms , Apoptosis , B7-H1 Antigen/genetics , B7-H1 Antigen/metabolism , Biomarkers, Tumor/metabolism , Hepatitis C/genetics , Humans , Oncogenes , Programmed Cell Death 1 Receptor , Proto-Oncogene Proteins c-bcl-2/genetics , Proto-Oncogene Proteins c-bcl-2/metabolism , Thyroid Neoplasms/pathology , Tumor Suppressor Protein p53/genetics
3.
Tissue Cell ; 48(3): 208-16, 2016 Jun.
Article in English | MEDLINE | ID: mdl-27036327

ABSTRACT

Ginger or Zingiber officinale which is used in traditional medicine has been found to possess antioxidant effect that can control the generation of free radicals. Free radicals are the causes of renal cell degeneration that leads to renal failure in case of gentamicin induced toxicity. This study was done to evaluate the possible protective effects of 6-gingerol as natural antioxidant on gentamicin-induced renal cortical oxidative stress and apoptosis in adult male albino rats. Forty adult male albino rats were used in this study and were randomly divided into four groups, control group; 6-gingerol treated group; gentamicin treated group and protected group (given simultaneous 6-gingerol and gentamicin). At the end of the study, blood samples were drawn for biochemical study. Kidney sections were processed for histological, and immunohistochemical examination for caspase-3 to detect apoptosis and anti heat shock protein 47 (HSP47) to detect oxidative damage. Gentamicin treated rats revealed a highly significant increase in renal function tests, tubular dilatation with marked vacuolar degeneration and desquamation of cells, interstitial hemorrhage and cellular infiltration. Immunohistochemically, gentamicin treated rats showed a strong positive immunoreaction for caspase-3 and anti heat shock protein 47 (HSP47). Protected rats showed more or less normal biochemical, histological, and immunohistochemical pictures. In conclusion, co-administration of 6-gingerol during gentamicin 'therapy' has a significant reno-protective effect in a rat model of gentamicin-induced renal damage. It is recommended that administration of ginger with gentamicin might be beneficial in men who receive gentamicin to treat infections.


Subject(s)
Antioxidants/administration & dosage , Catechols/administration & dosage , Fatty Alcohols/administration & dosage , Renal Insufficiency/drug therapy , Animals , Apoptosis/drug effects , Caspase 3/biosynthesis , Gentamicins/toxicity , HSP47 Heat-Shock Proteins/biosynthesis , Humans , Kidney/drug effects , Kidney/pathology , Male , Oxidative Stress/drug effects , Rats , Renal Insufficiency/chemically induced
4.
Int J Clin Exp Pathol ; 8(7): 7710-28, 2015.
Article in English | MEDLINE | ID: mdl-26339337

ABSTRACT

Alzheimer's disease (AD) is a neurodegenerative disorder with progressive degeneration of the hippocampal and cortical neurons. This study was designed to demonstrate the protective effect of caffeine on gene expression of brain derived neurotrophic factor (BDNF) and its receptor neural receptor protein-tyrosine kinase-ß (TrkB) as well as glial fibrillary acidic protein (GFAP) and Ki-67 immunoreactivity in Aluminum chloride (AlCl3) induced animal model of AD. Fifty adult rats included in this study were classified into 5 group (10 rats each); negative and positive control groups (I&II), AD model group (III), group treated with caffeine from the start of AD induction (IV) and group treated with caffeine two weeks before AD induction (V). Hippocampal tissue BDNF and its receptor (TrkB) gene expression by real time RT-PCR in addition to immunohistochemical study of GFAP and Ki67 immunoreactivity were performed for all rats in the study. The results of this study revealed that caffeine has protective effect through improving the histological and immunohistochemical findings induced by AlCl3 as well as BDNF and its receptor gene expression. It could be concluded from the current study, that chronic caffeine consumption in a dose of 1.5 mg/kg body weight daily has a potentially good protective effect against AD.


Subject(s)
Alzheimer Disease/drug therapy , Brain-Derived Neurotrophic Factor/metabolism , Caffeine/pharmacology , Gene Expression Regulation/drug effects , Signal Transduction/drug effects , Aluminum Chloride , Aluminum Compounds/adverse effects , Alzheimer Disease/chemically induced , Alzheimer Disease/metabolism , Animals , Brain-Derived Neurotrophic Factor/genetics , Chlorides/adverse effects , Disease Models, Animal , Glial Fibrillary Acidic Protein/genetics , Glial Fibrillary Acidic Protein/metabolism , Hippocampus/drug effects , Hippocampus/pathology , Humans , Ki-67 Antigen/genetics , Ki-67 Antigen/metabolism , Male , Neurons/drug effects , Neurons/pathology , Rats , Rats, Sprague-Dawley , Receptor Protein-Tyrosine Kinases/genetics , Receptor Protein-Tyrosine Kinases/metabolism
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