The rate of chronic kidney disease (CKD) is increasing globally, and it is caused by continuous damage to kidney tissue. With time the renal damage becomes irreversible, leading to CKD development. In females, post-menopause lack of estrogen supply has been described as a risk factor for CKD development, and studies targeting post-menopause CKD are scarce. In the present study, we used exosomes isolated from bone marrow mesenchymal stem/stromal cells (BM-MSCs) to test their therapeutic potential against the development of CKD. At first, the menopause model was achieved by surgical bilateral ovariectomy in female albino rats. After that, 100 µg of exosomes was given to ovariectomized rats, and the study continued for 2 months. Changes in urine volume, urine protein content, kidney function biochemical parameters (creatinine and BUN), kidney antioxidant parameters (SOD, GPx and CAT), histological changes, immunohistochemical levels of caspase 3, and the gene expression of NGAL (related to kidney damage), TGFβ1 and αSMA (related to fibrosis and EMT), and caspase 3 (related to apoptosis) were studied. After the ovariectomy, the occurrence of CKD was confirmed in the rats by the drastic reduction of serum estrogen and progesterone levels, reduced urine output, increased urinary protein excretion, elevated serum creatinine and BUN, reduced GPx SOD, and CAT in kidney tissue, degenerative and fibrotic lesions in the histopathological examination, higher immunohistochemical expression of caspase 3 and increased expression of all studied genes. After exosomes administration, the entire chronic inflammatory picture in the kidney was corrected, and a near-normal kidney structure and function were attained. This study shows for the first time that BM-MSCs exosomes are potent for reducing apoptosis and fibrosis levels and, thus, can reduce the chronic damage of the kidneys in females that are in their menopause period. Therefore, MSCs-derived exosomes should be considered a valuable therapy for preserving postmenopausal kidney structure and function and, subsequently, could improve the quality of females’ life during menopause.

The impact of microbial muramidase (MMUR) addition to broiler chicken rations was evaluated through growth parameters, liver histoarchitecture, antioxidant status, biochemical analysis, and expression of pro-inflammatory cytokines for 35 days. Four hundred three-day-old chicks (97.68 ± 0.59 g) were distributed to four distinct groups with ten duplicates each (100 chicks/group) consisting of: group 1 (G1): a basal diet without MMUR (control group); G2: a basal diet + 200 mg MMUR kg⁻¹ G3: a basal diet + 400 mg MMUR kg⁻¹; and G4: a basal diet + 600 mg MMUR kg⁻¹. The results showed that the final body weight and total weight gain were increased (p = 0.015) in birds fed with diets supplemented with MMUR at 600 mg kg⁻¹. The feed conversion ratio (FCR) was improved in all treatment groups compared with the control group. Birds fed with a diet supplemented with 600 mg MMUR kg⁻¹ showed the highest body weight gain and improved FCR. The values of thyroxin hormones and growth hormones were increased in all MMUR-supplemented groups. Dietary MMUR increased the activities of antioxidant enzymes (total antioxidant activity, catalase, and superoxide dismutase) and decreased the activity of malondialdehyde (p < 0.05). In addition, it increased the values of interleukin 1 beta and interferon-gamma compared with the control group. Furthermore, dietary MMUR increased the expression of transforming growth factor-beta immunostaining in the liver and spleen tissues. Our results show that supplementing broilers’ diets with 600 mg MMUR kg⁻¹ could enhance the chicken growth rate and improve their antioxidant, inflammatory, and anti-inflammatory responses.

Brain is the central organ in human body, that is working 24hr/7days even before we leave our mother`s womb. None surprising that care should be paid for the food consumed that consequently affecting brain environment, neurotransmitters as well as oxidative state. Carmoisine (Car) and sunset yellow (SY) are synthetic food additives extensively utilized during food processing and subsequently affecting brain health. The apoptotic effect underling the behavioral changes after oral consumption of either Car or SY remains not fully understudied. Respective biochemical and molecular biological parameters by means of one fifty adult male mice were conducted. The study extended for 3 months on 5 different groups with ten mice each; Group 1 was utilized as the control group, group 2 was treated with the acceptable daily intake (ADI) of SY (30 mg/kg BW), group 3 was treated with 10x ADI of SY, group 4 was treated with ADI of Car (4 mg/kg BW) and group 5 was administered 10x ADI of Car; all doses were given orally via gastric lavage. Exposure to higher doses of either SY or Car significantly altered the biochemical parameters; decreased both serotonin and dopamine levels and total antioxidant capacity as well. However, increased the lipid peroxidation marker malonaldehyde (MDA), upregulated the mRNA expression of the pro-apoptotic genes (Fas, Fas-L, Bax and casp3) and down regulated the transcriptional level of the anti-apoptotic gene Bcl2.Moreover upregulated both miR-140 and miR-34a expression levels and consequently down-regulated their target genes NRF-2 and SIRT-1, respectively. So, we can conclude that excessive oral administration of either Car or SY has apoptotic effect and care should be paid with their usage.

Exosomal microRNAs have been attracting major interest as potential diagnostic biomarkers for metabolic syndrome. The aim of our study was to characterize the serum exosomes, exosomal miRNA and their target genes to identify those that were altered in relation to different conditions of metabolic syndrome with different forms of treatment to evaluate their use as diagnostic and treatment biomarkers; Eighty male adult albino rats were used in this experiment, 10 served as control group and other 70 divided into 7 different groups, some served as metabolic syndrome models without treatments and others were served as metabolic syndromes models with different treatments. Our results explained that, the expression levels of miR-122, sterol response elementary binding protein-1 (SREBP-1) & fatty acid synthase-1 (FAS-1) were significantly higher in the hepatic tissue of metabolic syndrome model groups than that of control and significantly down-regulated after different treatments but still higher than that of control group while carnitine palmitoyltransferase-1(CPT-1) was significantly decreased in the same groups. Also the expression levels of miR-31 was significantly higher in Adipose tissue of metabolic syndrome model groups than that of control and significantly down-regulated after different treatments but still higher than that of control group while Leptin gene (Ob), Phosphoinositide-3-kinase, class 2, alpha polypeptide (PIK3C2A) and Peroxisome proliferator-activated receptor-γ (PPAR-γ) were significantly decreased in the same groups. It was concluded that Exosomal miRNA signatures appear to mirror pathological changes of metabolic syndrome patients and several miRNAs are promising biomarkers for non-invasive diagnosis of the disease.