Aging represents a complex biological process associated with decline in skeletal muscle functions. Aging impairs satellite cells that serve as muscle progenitor cells. Probiotic supplementation may have many beneficial effects via various mechanisms. We examined the possible effects of probiotics in stimulating the proliferation of myogenic stellate cells in aging rats. Twenty-four male albino Sprague–Dawley rats were classified equally into four groups: adult control, old control, adult + probiotics, and old + probiotics. Probiotics (Lactobacillus LB) were administered gavage at a dose of 1 ml (1 × 10⁹ CFU/ml/day) for 4 weeks. A significant increase in the relative gastrocnemius weight ratio and improvement of contractile parameters was detected in the old + probiotics group (0.6 ± 0.01) compared to the old control group (0.47 ± 0.01; P < 0.001). Probiotics significantly upregulated the activities of GSH, while NO and MDA were markedly decreased compared to control groups (P ≤ 0.001). Also, probiotics increased the mRNA and protein expressions of myogenin and CD34 (P < 0.05) as determined by real-time PCR and immunohistochemistry. Moreover, the old + probiotics group showed apparent restoration of the connective tissue spaces, reflecting the all-beneficial effects of probiotics. Our findings indicated that probiotics attenuated myopathic changes in aging rats probably through activation of the myogenic stellate cells. Probiotics improved the muscle weight, function, antioxidant activity, and myogenic transcription factors of the skeletal muscle.

Background: Plastic is one of the most versatile and widely used materials, but the environmental accumulation of nanoplastics (NPs) poses a risk to human health. Preclinical studies have verified that the liver is one of the main organs susceptible to NPs. Biobran/MGN-3, an arabinoxylan from rice bran, has been shown to have hepatoprotective effects; here, we show Biobran’s ability to alleviate polyethylene nanoplastics (PE-NPs)-induced liver cell toxicity by reversing apoptosis and restoring G2/M cell arrest in mouse liver cells (BNL CL.2). Methods: Toxicological effects were measured using the sulforhodamine B (SRB) assay for cell viability and flow cytometry for cell cycle analysis and apoptosis. An in silico study was also used to demonstrate the docking of PE-NPs to pro-inflammatory mediator proteins (IL-6R, IL-17R, CD41/CD61, CD47/SIRP), cell cycle regulators (BCL-2, c-Myc), as well as serine carboxypeptidase, which is an active ingredient of Biobran. Results: Exposing liver cells to PE-NPs caused a significant decrease in cell viability, with an IC50 value of 334.9 ± 2.7 µg/mL. Co-treatment with Biobran restored cell viability to normal levels, preserving 85% viability at the highest concentration of PE-NPs. Additionally, total cell death observed after exposure to PE-NPs was reduced by 2.4-fold with Biobran co-treatment. The G2/M arrest and subsequent cell death (pre-G0 phase) induced by PE-NPs were normalized after combined treatment. The in silico study revealed that Biobran blocks the nucleophilic centers of PE-NPs, preventing their interaction with pro-inflammatory mediators and cell cycle regulators. Conclusions: These findings highlight the potential use of Biobran as a hepatoprotector against NP toxicity.

Background: The molecular basis of pancreatic steatosis is not entirely known. Aquaporins (AQPs) are integral membrane proteins involved in a variety of pancreatic functions. Given the little data regarding the potential role of aquaporins in the pathogenesis of pancreatic steatosis, this study was designed to assess the role of aquaporins and the NLRP3-inflammasome in the rat model of high-fat fructose diet (HFFD) and to investigate the impact of vitamin D supplementation and alternate day fasting (ADF) in ameliorating HFFD-induced pancreatic steatosis. Method: Twenty-four Sprague-Dawley male rats were divided equally into 4 groups. Group I (control group), Group II (HFFD group), Group III (HFFD + ADF group), and Group IV (HFFD + vitamin D group). By the end of the experiment, fasting blood samples were collected for determination of blood glucose, serum insulin, lipid profile, and insulin resistance. Oxidative stress biomarkers (malondialdehyde and reduced glutathione), inflammatory markers (interleukin-1β and TNF-α), and expression of aquaporins (AQP-1, AQP-3, and AQP-7) genes were evaluated in pancreatic tissues. Histopathological examination of the pancreas and immunohistochemistry of the NLRP3-infammasome and AQP-7 were performed. Results: The HFFD group exhibited pancreatic steatosis with a significant elevation in the levels of blood sugar, serum insulin, insulin resistance, lipid profile, oxidative stress, inflammatory markers, and AQP-3 and AQP-7 mRNA expressions. Regarding histopathology, there were pale vacuolated-stained cytoplasm in acinar pancreatic cells and increased immunoreactivity for AQP-7 and NLRP3-inflammasome. All these parameters improved with ADF and vitamin D supplementation, with more favorable effects for ADF. Conclusion: ADF and vitamin D treatment ameliorated the effect of the high-fat fructose diet at both levels of the biochemical and histopathological examinations.