Reports of Biochemistry and Molecular Biology最新文献

Background: Chemical agents, such as Chlorhexidine are used as one of dental plaque control strategy. Researchers are looking for a natural and economic substitute with same antibacterial efficacy and less complications. The aim of this study was to evaluate the antimicrobial efficacy of the Khorasan Razavi walnut green husk (WGH) extract with and without adding ZnO nanoparticles (nZnO) on Streptococcus mutans (S. mutans).

Methods: In this in vitro study, antimicrobial effect of the Hydro-ethanolic extract of WGH, was evaluated against S. mutans. Broth Dilution and Agar diffusion methods were used with 90 tubes containing different dilutions of WGH extract (100 to 0.006 mg/ml). ZnO nanoparticles (nZnO) were added to 45 tubes. Streptococcus mutans was exposed to 15 different serial concentrations of study extracts, from 100 mg/ml to 0.006 mg/ml. Minimum inhibitory concentration (MIC) of the study extracts were determined and zone of inhibition diameter was compared to positive controls (chlorhexidine 0.2%, nZnO), and negative control (sterile distilled water). The differences between the mean diameters, were analyzed by independent sample T- teS.

Results: Minimum inhibitory concentration (MIC) of study extract was found to be 50mg/mL, with adding nZnO, MIC was reduced to 3.12mg/mL. Mean diameter of inhibition zone at 3.12 mg/ml with and without adding ZnO nanoparticles were 17.67±0.57 mm and 8±0.001 mm, respectively, (p-value< 0.001).

Discussion: Adding nZnO could be enhanced antimicrobial efficacy of the WGH extract against S. mutants, while it was still less effective than chlorhexidine.

Background: Recent research indicates that persistent inflammatory responses may contribute to the rise of diabetic nephropathy (DN) and diabetic cardiovascular disease (DCVD) in type 2 diabetes mellitus patients (DM2). Numerous molecules associated with inflammation and angiogenesis have been implicated in the development and progression of DN and DCVD, respectively.

Methods: The subjects were separated into five groups: healthy controls (n= 25), type 2 diabetes mellitus patients (n= 30), type 2 diabetes mellitus patients with nephropathy DN (n= 30), and type 2 diabetes mellitus patients with cardiovascular disease DCVD (n= 30). The blood levels of irisin, IL-8, HbA1C, urea, and creatinine were determined.

Results: In current study there was high significant increased irisin levels (p< 0.001) in DN patients than other groups and a high significant decreased IL-8 level in DCVD.

Discussion: Serum IL-8 and irisin levels may serve as early indicators of DM2 problems (DN, DCVD).

Background: Psoriasis is a chronic inflammatory immune mediated disease arising from interaction between genetic risk variants and the environment. Maternally expressed gene3 (MEG3) is a long noncoding RNA (lncRNA) known for gene transcription regulation and inhibiting proliferation. MEG3 competes with microRNA (miRNA-21) influencing cell proliferation and apoptosis balance. Endoplasmic reticulum (ER) stress proteins promote cell survival via unfolded protein response (UPR) influenced by MEG3. We aimed to detect the possible role of MEG3, miRNA-21 and ER stress proteins in pathogenesis of psoriasis vulgaris.

Methods: Human GRP78, ATF6, caspase3 tissue levels were assayed by Enzyme Linked Immunosorbent Assay (ELISA). Assessment of long non-coding MEG3 and miRNA 21 expressions was done by quantitative real time polymerase chain reaction (qRT-PCR).

Results: Expression of MEG3 was significantly downregulated, while miRNA-21 was remarkably upregulated, ER stress proteins GRP78, ATF6, and caspase 3 all showed low levels in homogenized psoriatic lesions when compared to normal skin. miRNA 21 and MEG3 were identified as possible diagnostic markers for psoriasis vulgaris.

Discussion: MEG3 is barely expressed in psoriatic lesions while miRNA-21 expression is remarkably elevated but when correlated to each other there was unexpected positive correlation. MEG3 and miRNA-21 were identified as possible diagnostic markers for psoriasis. Undifferentiated psoriatic lesions have very weak UPR.

Background: Infection with COVID-19 can cause hepatic damages. Here, we aimed to examine the effect of COVID-19 infection on the serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), albumin, and procalcitonin (PCT) concentrations as markers to evaluate the liver function.

Methods: In this study, 56 patients infected with COVID- 19 and 28 healthy controls was recruited in Private Nursing Home Hospital of the Medical City, Baghdad. Patients were subdivided according to disease severity into severe and non-severe groups.

Results: The results showed that the mean±SD value of serum AST activity and serum PCT concentrations were elevated significantly in severe group in comparison to healthy control, (p< 0.01, p< 0.001) respectively. Also, the mean ±SD value of serum ALT activity was higher in severe group compared to the healthy subjects and non-severe ones, significantly (p< 0.0001, p< 0.003) respectively. While the mean value of serum albumin concentration of severe patients and non-severe group were significantly decreased compared to healthy subjects. The receiver operating characteristic curve (ROC) revealed that ROC value of albumin (0.992) differentiates between non-severe infected patients and healthy subjects, while the ROC value of serum ALT activity (0.735) differentiates between severe COVID-19 patients and non- severe ones.

Conclusion: Changes of liver function parameters in COVID-19 patients were mild to moderate and measurement of serum ALT activity is the best biomarker in differentiation between non-severe patients and severe ones and albumin concentration is excellent in discrimination between patients and controls.

Background: Colorectal cancer (CRC) is still considered one of the prevalent cancers worldwide. Investigation of potential biomarkers for early detection of CRC is essential for the effective management of patients using therapeutic strategies. Considering that, this study was aimed to examine the changes in lncRNA FOXD2-AS1 expression through colorectal tumorigenesis.

Methods: Fifty CRC tumor tissues and fifty adjacent normal tissue samples were prepared and involved in the current study. Total RNA was extracted from the samples and then reverse transcribed to complementary DNA. Next, the expression levels of lncRNA FOXD2-AS1 were evaluated using real-time PCR in CRC samples compared to normal ones. Also, receiver operating characteristic curve analysis was used to evaluate the diagnostic value of FOXD2-AS1 for CRC.

Results: The obtained results showed that the expression level of FOXD2-AS1 gene was significantly (p<0.0001) up-regulated in tumor tissues compared to normal marginal tissues. Also, a significant correlation was observed between higher the expression of FOXD2-AS1and the differentiation of tumor cells. Furthermore, ROC curve analysis estimated an AUC value of 0.59 for FOXD2-AS1, suggesting its potential as a diagnostic target.

Conclusion: Taken together, the current study implied that tissue-specific upregulation of lncRNA FOXD2-AS1 might be appropriate diagnostic biomarkers for CRC. Nonetheless, more studies are needed to validate these results and further illustrate FOXD2-AS1 function through colorectal tumorigenesis.

Background: Bladder cancer is one of the most common genitourinary cancers with significant mortality. Finding reliable tumor markers and potential drug targets can improve early diagnosis, prognosis, and more effective therapeutic protocols. Previous studies have reported the involvement of the substance P (SP)/neurokinin-1 receptor (NK-1R) system in cancers. The potential prognostic role and the interaction of SP and NK-1R in bladder tumor are yet to be elucidated.

Methods: Serum samples from 22 primarily diagnosed patients with bladder cancer as well as 22 healthy controls were examined for SP level using ELISA method. Tissue distribution of NK-1R in tumor samples and their adjacent normal tissues was evaluated through immunohistochemistry.

Results: Serum SP levels in patients with bladder cancer were higher than the healthy group (p< 0.001) and had a significant correlation with NK-1R staining intensity (p< 0.001), percentage of stained cells (p< 0.001), and NK-1R tissue distribution. Also, the immunoreactivity of NK-1R in cancer samples increased significantly without correlation with tumor characteristics. However, no significant association was found between SP and NK-1R levels with clinical characteristics including tumor size (p= 0.33), tumor stage (p= 0.29), grade (p= 0.93), NK-1R staining intensity (p= 0.53), and percentage of stained cells (p= 0.32).

Discussion: According to our findings, despite the lack of association between SP and NK-1R with clinical characteristics of bladder cancer, their serum levels were higher in patients with bladder cancer. Further studies are needed to confirm the potential prognostic role of SP and NK-1R in bladder cancer.

Background: Chronic kidney disease (CKD) is a global health concern involving roughly one-tenth of developed countries' populations. The flavin-containing dimethylaniline monooxygenase 3 (FMO3) gene encodes an enzyme that catalyzes trimethylamine N-oxide (TMAO), a toxin in CKD sufferers. This preliminary study aims to evaluate the association between coding region variations of FMO3, rs2266782G/A (E158K), rs2266780A/G (E308G), and rs1736557G/A (V257M), and the susceptibility to CKD.

Methods: A total of 356 participants were enrolled, including 157 patients diagnosed with CKD and 199 age-matched healthy individuals. Genotyping of FMO3 gene variations was performed via PCR-RFLP and ARMS-PCR methods.

Results: Our findings revealed a significant association between rs2266780A/G and rs1736557G/A and CKD under different genetic models. Compared to the GGG haplotype of rs2266782/rs1736557/rs2266780, the GAG, GAA, AAG, and AAA haplotype combinations conferred an increased risk of CKD in our population. Interaction analysis revealed that some genotype combinations, including GA/AA/AA, AA/AA/AA, GA/AA/GA, and GG/AG/AA, dramatically increased CKD risk in the Iranian population. No correlation was found between FMO3 polymorphisms and CKD stages.

Discussion: These observations highlight the potential impact of coding variants of the FMO3 gene on the onset of CKD. Further investigations into expanded populations and diverse races are needed to confirm our findings.

Background: Receptor advanced glycation end products (RAGE) activation plays an essential role in diabetic retinopathy (DR) progression. This study was aimed to explore the role of anti-RAGE antibodies (RAGE antagonists) in inhibiting DR progression through their hypoglycemic and anti-inflammatory mechanism in diabetic retinopathy induced rats.

Methods: A total of 30 male Wistar rats were randomly divided into five group. The group was consisted of normal control group, DR group without treatment, DR group with anti-RAGE 1 ηg/kg BW, 10 ηg/kg BW, and 100 ηg/kg BW. To assess the diabetic retinopathy, fundus photographs were taken every week using a camera with 16x magnification placed in front of the rat's eyes. Blood glucose was checked by the glucose oxidase-peroxidase method. Retinal TNF-α levels and VEGF were examined using an enzyme-linked immunosorbent assay (ELISA) kit.

Results: The finding of this study showed that anti-RAGE treatment at dose of 10 and 100 ηg/kg BW, HbA1c levels were significantly higher (p< 0.05) compared to the normal control group but significantly lower (p< 0.05) than in the diabetes group. The mean blood vessel diameter in the DR+anti-RAGE 10 and 100 ηg/kg BW groups was significantly lower than in the diabetic retinopathy group (p< 0.05). The administration of anti-RAGE 10 and 100 ηg/kg BW showed the ability to significantly reduce VEGF levels compared to the DR group (p< 0.05).

Discussion: This study revealed at doses of 10 and 100 ηg/kg BW, anti-RAGE antibodies improved diabetic retinopathy in Wistar rats through hypoglycemic effects and anti-inflammatory mechanisms.

Background: MicroRNA is a form of non-coding RNAs that able to regulate gene expression. miR-424 is one of the members of the regulatory family, which plays an important role in the proliferation and differentiation of myeloid cells. Epigenetic changes can change the level of miR-424 under environmental factors. Therefore, the level of expression of miR-424 in U937 cells of the myeloid line was evaluated in this research under the influence of vitamin D3 (VitD3) and retinoic acid (RA).

Methods: In this study, U937 cells were cultured in the presence of VitD3, and RA to evaluate cell proliferation, viability via the trypan blue exclusion test, and expression level of miR-424 by real-time PCR at specific times.

Results: Cell proliferation has shown a significant decrease in the RA group versus other groups during incubation times (P < 0.05). In VitD3 group, there was a significant increase in cell proliferation after 24- and 48-hours incubation periods versus other groups. In the VitD3 and RA groups, the increase of cell proliferation caused the downregulation of miR-424. In addition, the upregulation of VitD3 group and downregulation of the RA group were significant versus the control group (P < 0.05).

Discussion: We concluded that the expression level of miR-424 was critically affected in the dose- and time-dependent of RA and VitD3 treatment in the U937 cell line. Treatment with VitD3 decreased the expression of miR-424 and RA treatment increase miR-424 expression level in physiological doses.