Background: Aging is associated with impaired renal function and structural alterations. Oxidative stress plays a vital role in renal senescence and damage. Sirtuin 1 (SIRT1) is thought to protect cells from oxidative stress through nuclear factor erythroid 2-related factor 2 (NRF2). Ellagic acid (EA), a natural antioxidant, has been demonstrated to have renoprotective roles in vitro and in vivo. This study investigated if SIRT1 and NRF2 mediate the protective effects of EA in aged kidneys. Methods: Male Wistar rats were divided into three groups including young (4 months), old, and old + EA (25 months). Young and old groups received EA solvent, while the old + EA group was treated with EA (30 mg/kg) by gavage for 30 days. Then, the level of renal oxidative stress, SIRT1 and NRF2 expression, kidney function parameters, and histopathological indices were measured. Results: Treatment with EA significantly increased the level of antioxidant enzymes and reduced malondialdehyde concentration (P < 0.01). Moreover, EA administration remarkably upregulated mRNA and protein levels of SIRT1 and NRF2 as well as deacetylated NRF2 protein (P < 0.05). Additionally, EA treated rats improved kidney function and histopathological scores (P < 0.05). Conclusions: These findings suggest that ellagic acid exerts protective effects on aged kidneys by activating SIRT1 and NRF2 signaling.

Ellagic acid is used in traditional medicine for the treatment of lipid disorders. In this study, the effects of ellagic acid on key regulators of lipid metabolism, and histopathological alterations in aged liver were examined. A total of 21 male Wistar rats were divided into three groups, including young control, old control, and old ellagic acid. After one month of treatment with ellagic acid, the expression levels of hepatic SIRT1, AMPK, SREBP-1c, PPAR-α, and phosphorylated AMPK (p-AMPK) were evaluated. The levels of several serum biochemical factors, and hepatic triglyceride, and cholesterol contents were assessed. Ellagic acid elevated the levels of SIRT1, p-AMPK, and PPAR-α and reduced SREBP-1c level in the liver of old rats. It decreased triglyceride and cholesterol contents in the aged liver and improved histopathological changes. The results demonstrated that ellagic acid can exert protective effects against hepatic lipid metabolism disorders induced by ageing.

Prolactin (PRL) is secreted by various cells in the anterior pituitary gland, mammary glands, placenta, uterus, ovaries, testes, skin, adipose tissue, endothelial cells, immune system, and central nervous system. The expression and secretion of PRL are influenced by several factors such as suckling, thyrotropin‐releasing hormone (TRH), cytokines, dopamine, estrogen, and vasoactive intestinal polypeptide. It operates through a complex receptor, which is expressed in mammary gland cells, pancreatic beta cells, adipocytes, and immune cells. PRL is essential for various physiological functions, in particular milk production, breast development, metabolism, and immune regulation. Serum PRL levels fluctuate daily and can be affected by exercise, diet, and stress. Hyperprolactinemia is linked to autoimmune diseases and viral infections. In viral infections such as HIV, HCMV, HCV, and COVID‐19, PRL levels are often increased, which may influence the immune responses. PRL can modulate the activity of various immune cells, including T cells, B cells, natural killer cells, and macrophages, mounting an effective immune response against viral infections. Moreover, PRL influences the production of cytokines that mediate and regulate immunity and inflammation. PRL stimulates B cells to produce antivirus antibodies that are essential for neutralizing viruses and preventing their spread within the body. PRL levels, varying by sex and life stage, may affect immune responses and susceptibility to viral infections. Moreover, overexpression of PRL was indicated in various autoimmune diseases. Overall, PRL is a complex hormone with significant implications for endocrine function, immune regulation, and immune responses to viral infections, highlighting the need for further research into its diverse roles in health and disease. This review summarizes current knowledge of the immunomodulatory effects of PRL in human viral infections and possibly its contribution to the development of autoimmune diseases.

Dyslipidemia is a major modifiable risk factor for cardiovascular disease (CVD). While thyroid dysfunction is a well-established secondary cause of dyslipi

Background: Aging is associated with chronic diseases and increased oxidative stress, particularly affecting liver function. Aging is linked to chronic diseases and heightened oxidative stress, particularly impacting liver function. Recent research has demonstrated that oral administration of trehalose offers multiple benefits for various tissues and organs. Methods: This study investigated the effects of oral trehalose (2% in water) on the gene expression of key markers linked to liver oxidative stress and inflammation in 4-month-old adult and 24-month-old Wistar rats. Thirty-two male Wistar rats (n=8) were randomly assigned into four groups: adult control, aged control, adult trehalose (2% in water), and aged trehalose, over a treatment period of one month. Following treatment, liver tissues were analyzed using real-time PCR for genes related to oxidative stress (PGC-1α, NRF2, and SOD) and inflammation (NF-κB, IL-1β, TNF-α, and TGF-β). Results: Our findings revealed a significant up-regulation of PGC-1α, NRF2, and SOD in aged trehalose group compared to the aged control (P<0.001); however, SOD expression increased by trehalose administration in aged rats compared to other 3 groups. Inflammatory markers (NF-κB, IL-1β, TNF-α) were significantly reduced by trehalose, and TGF-β expression, involved in fibrosis, was attenuated exclusively in aged rats compared with controls (P<0.05). Conclusion: These results suggest that trehalose has a protective effect on hepatic function, particularly in the aging population, and highlight its potential therapeutic role in age-associated liver dysfunction.