Archives of Physiology and Biochemistry最新文献

This study investigated the anti-atherogenic effects of Plectranthus glandulosus leaves aqueous, hydro-ethanolic extracts, and ethyl acetate fraction at doses of 100, 200, and 400 mg/kg for 21 d. As results, at the dose of 400 mg/kg, the ethyl acetate fraction significantly (p < .001) decreased the level of total cholesterol (112.52 ± 1.21 mg/dL), triglyceride (76.47 ± 0.97 mg/dL), and LDL-C (22.01 ± 2.92 mg/dL). Whereas, a significant (p < .001) increase was observed in the level of HDL-C (74.97 ± 1.99 mg/dL). Moreover, the atherogenic index significantly (p < .001) decreased (0.008 ± 0.00 mg/dL), while the percentage of atherogenic protection increased (99.13 ± 0.78%). The activity of antioxidant enzymes increased significantly (p < .001), while malondialdehyde concentration decreased. The thickening of aorta media (67.27 ± 7.15 µm) was also attenuated significantly (p < .001). Thus, our finding supports the use of Plectranthus glandulosus for future atherosclerosis drug discovery.

Objective: This study was to investigated the inhibitory role of the tumour protein p53 (TP53)-activated PGM5-AS1 in lung cancer (LC) cell proliferation, invasion, and CSC-like properties and its underlying mechanisms.

Methods: The effect of PGM5-AS1 on LC cell development was determined. Stem cell markers, aldehyde dehydrogenase activity in cells were tested, as well as the ability of stem cells to form spheroids. The interaction of PGM5-AS1 and TP53 was determined. The binding link of PGM5-AS1, miR-1247-5p, and R-spondin1 (RSPO1) was verified.

Results: PGM5-AS1 was elevated by a combination of TP53 and PGM5-AS1 promoters. PGM5-AS1 was a molecular sponge of miR-1247-5p in LC cells, and miR-1247-5p targeted RSPO1. Elevating PGM5-AS1 or repressing miR-1247-5p restrained LC cell growth and stemness, which were reversed by depression of RSPO1.

Conclusion: This study conveys that TP53-elevated PGM5-AS1 mediates miR-1247-5p to target RSPO1, thereby inhibiting LC growth and stemness, representing a novel avenue for LC therapy.

Objective: This study explores the mechanism of methyltransferase like 3 (METTL3) on sepsis-associated encephalopathy (SAE)-induced hippocampal neuronal injury.

Methods: A murine model of SAE was established by caecal ligation and puncture. Hippocampal cells were induced by lipopolysaccharide (LPS). The mouse survival was observed and behavioural tests evaluated cognitive function. METTL3 and glutamic-oxaloacetic transaminase 1 (GOT1) expressions were detected via RT-qPCR and Western blot. Immunofluorescence staining examined the co-localization of NeuN and METTL3. The m6A enrichment on GOT1 was determined by MeRIP.

Results: METTL3 and GOT1 were highly expressed in SAE mice and LPS-stimulated hippocampal cells. SAE mice exhibited cognitive function impairment, reduced survival rate, and decreased neuronal cells. LPS induction increased hippocampal cell apoptosis and enhanced inflammation. Silence of METTL3 reduced hippocampal neuronal injury in SAE mice and LPS-induced hippocampal cell injury.

Conclusion: METTL3-mediated m6A modification on GOT1 mRNA elevates GOT1 expression, thereby aggravating SAE-induced hippocampal neuronal injury.

Introduction: This study aimed to assess the expression changes of BTG1, PGI, and PGII in tissues and serum of patients with gastric cancer, atrophic gastritis, and healthy individuals.

Methods: QRT-PCR was used to measure BTG1, PGI, and PGII expression in 30 cancers, 30 atrophic gastritis, and 30 healthy tissue samples. Serum levels of PGI and PGII were measured using ELISA. Statistical tests included the Mann-Whitney U and independent T-test. Covariates like tumour stage and H. pylori status were considered.

Results: BTG1 expression was significantly lower in cancer and gastritis tissues. Serum PGI and PGII levels were significantly reduced in cancer patients (P ≤ 0.001).

Discussion: The PGI/PGII ratio in serum emerged as a strong non-invasive biomarker for distinguishing cancer from healthy individuals. While BTG1 provides insights into gastric carcinogenesis, its clinical utility is limited due to the need for tissue samples. The serum-based PGI/PGII ratio shows greater promise as a non-invasive screening tool for GC.

Diabetic retinopathy (DR) is the leading manifestation of diabetic microangiopathy. However, effective biomarkers and therapies are lacking. Circular RNAs (circRNAs) have been implicated in various diseases including DR. However, the role of circRNAs in DR remains elusive. In the present study, circNXN was upregulated in high glucose (HG)-treated human retinal microvascular endothelial cells (hRMECs). circNXN knockdown inhibited the proliferation, migration, and angiogenesis of hRMECs and promoted apoptosis. In addition, circNXN acted as a sponge for miR-338-3p to facilitate the FGFR1 (fibroblast growth factor receptor 1) expression. Furthermore, rescue assays revealed that the reduced promoting effect on hRMECs induced by the knockdown of circNXN could be reversed by a miR-338-3p inhibitor in HG-treated hRMECs. Additionally, in a DR rat model, circNXN downregulation ameliorated retinal vasculature changes. Our findings reveal a new therapeutic strategy for DR that may provide a new approach to clinical DR therapy.

Objective: This study investigated bee bread's (BB) protective and therapeutic effects on acetic acid-(AA)-induced gastric ulcers via oxidative stress, DNA damage, inflammation, and apoptosis.

Materials and methods: Rats were administered saline-(1ml) or BB-(0.5g/kg/day;1ml) by oral gavage once daily for 10-day following 80% AA-induced chronic ulceration in treatment group. Pretreatment group received saline or BB for 10-day before and 3-day after ulcer induction. Stomachs of decapitated rats were collected for ulcer index, histological and biochemical analyses.

Results: BB significantly reduced the gastric ulcer index and levels of chemiluminescence, HMGB-1, IL-6, IL-1ß and IL-8 levels in pretreatment and treatment groups. In BB-pretreated ulcer group, MPO-(salineBB, 39.9±3.7 U/g;22.2±2.2 U/g), caspase-3 (0.40±0.07 ng/g;0.18±0.01 ng/g) and IFN-γ (15.46±1.76;9.51±1.95 ng/g) levels decreased and TNF-α (31.77±5.13;18.94±2.59 ng/g) reduced only in BB-treated ulcer group. MDA, GSH, NRF-2, and 8-OHdG levels remained unchanged.

Conclusion: BB has demonstrated protective and therapeutic effects by reducing ROS production, modulating inflammation and apoptosis.

Gestational diabetes mellitus (GDM) is one of the most prevalent metabolic diseases in pregnant women. In this study, we investigated the effects of Salusin-α in rodent models of GDM. We observed decreased levels of Salusin-α in the placental tissue of GDM mice. Salusin-α alleviated GDM symptoms by reducing blood glucose and increasing serum insulin levels. Further analysis revealed that Salusin-α improved lipid profiles and foetal outcomes in GDM mice. Additionally, Salusin-α mitigated oxidative and nitrosative stress in the placental tissue of GDM mice by enhancing the levels of Vitamin E, Vitamin C, and reduced GSH, while decreasing levels of TBARS and nitric oxide metabolites (nitrite + nitrate = NOx). Salusin-α also reduced the levels of MCP-1 and IL-8. Mechanically, Salusin-α inhibited the activation of p38/NF-κB by reducing phosphorylated p38 and phosphorylated NF-κB p65. In conclusion, our findings support the potential clinical application of Salusin-α as a novel peptide for molecular intervention in GDM.

The aim of this study is to examine the effects of cinnamon and statins on the renal and liver functions of gentamicin-received rats.

Methods: Forty male albino rats were recruited into 4 groups (10 rat each) for a 21-day period by gavage treatment. The control group 1 was given nothing but 0.5 ml normal saline, and others injected with a dose of 100 mg/kg of Gentamicin intraperitoneally for one week before treatment. Group 2 received Gentamicin alone, Group 3 received an aqueous extract of cinnamon, and Group 4 treated with a statin medication.

Results: Gentamicin-treated group compared to other groups showed a significant increase in lever and kidney enzymes. The group treated with cinnamon or statin revealed noticeable positive effects on these markers, whereas statin showed decrease in Alanine Aminotransferase ALT levels.

Conclusion: Parameters of hepatotoxicity and nephrotoxicity induced by gentamicin were significantly reserved by cinnamon or statin, statin less effective.

Objective: Maximum-voluntary-ventilation (MVV) is the maximal volume of which an individual can move by voluntary effort in one minute. It is possible that the first second forced-expiratory-volume (FEV₁) could be more to reliable assess respiratory muscle endurance to estimate MVV.

Methods: For this aim, 422 athletes (Age 22.9 ± 8.5 years; 98/324 - females/males) were performed a MVV, and FEV₁ measurements.

Results: The coefficient of determination was R² = 0.594 between MVV and FEV₁, with a predictive equation for overall participants: MVV = (FEV₁ × 33.5)+12.7. The robust regression showed a good multiple correlation coefficient (R = 0.815) with the coefficient of determination R² = 0.661 for the model including FEV₁, age and gender as predictors. These equations MVV = (FEV₁ X 27.3)+(Age(y) × 1.1)+20.5 and MVV = (FEV₁ × 27.3)+(Age(y) × 1.1) were derived for male and female, respectively.

Conclusion: FEV₁ can predict MVV in different athletes with greater accuracy when stratified per gender. Therefore, this new approach can be used in a short all-out test without stress of the respiratory muscle to predict MVV in athletes.

Methods: This case-control study looked at a total of 104 university students, 51 individuals with obesity, and 53 individuals as controls. Biochemical measurements by the colorimetric method include zinc and copper. Genetic analysis by the tetra primers ARMS-PCR was used for genotyping the rs180113 SNP in the MTHFR gene.

Results: Serum zinc levels were significantly higher in the obese group compared to the non-obese group (145.1 ± 24.89 ug/dl vs. 114.8 ± 29.44 ug/dl, p = 0.0133), while copper levels showed no significant difference. Genotyping revealed the rs1801133 polymorphism in the MTHFR gene is significantly associated with obesity, with the A allele more frequent in obese individuals (39.6% vs. 14.5%, p < 0.05).

Conclusion: Zn and rs1801133 are associated with obesity, the A allele of rs1801133 SNP and the significant associations observed in different genetic models highlight the potential of this polymorphism as a genetic marker for obesity risk.