Ulcerative colitis is a common intestinal inflammatory disease characterized by upregulation of pro-inflammatory cytokines and oxidative stress. Zeaxanthin is a nutritional carotenoid that belongs to the xanthophyll family of pigments. It exerts potent anti-inflammatory and antioxidative effects. The present study aimed to evaluate the effect of zeaxanthin on acetic acid-induced ulcerative colitis in rats. Rats were randomly categorized into five groups: control, zeaxanthin, acetic acid, acetic acid + zeaxanthin, and acetic acid + prednisolone groups. Zeaxanthin (50 mg/kg/day) or prednisolone (5 mg/kg/day) was orally administered for 14 days before induction of ulcerative colitis. On the 15th day, colitis was induced by transrectal administration of 3% acetic acid. The rats were sacrificed 24 h after rectal instillation and their colon tissues were examined. Pretreatment with zeaxanthin significantly reduced disease activity index, wet colon weight, ulcer area, macroscopic scores, and histological changes. Zeaxanthin also effectively downregulated the levels of myeloperoxidase and malondialdehyde, upregulated the enzymatic activity of superoxide dismutase and catalase, and raised glutathione levels. With regard to anti-inflammatory mechanisms, zeaxanthin suppressed tumor necrosis factor-alpha, interferon-gamma, interleukin-6, interleukin-1 beta, and nuclear transcription factor kappa B levels, and inhibited nitric oxide synthase and cyclooxygenase-2 protein expression. Our results indicate that oral administration of zeaxanthin ameliorates acetic acid-induced colitis in rats via antioxidative effects and modulation of pro-inflammatory cytokine and mediator activity. Therefore, zeaxanthin may be an effective therapeutic candidate for the treatment of ulcerative colitis.

Objective: Diabetes mellitus causes deterioration in the body, including serious damage of the oral cavity related to salivary gland dysfunction, characterised by hyposalivation and xerostomia. Human dental pulp stem cells (hDPSCs) represent a promising therapy source, due to the easy, minimally invasive surgical access to these cells and their high proliferative capacity. It was previously reported that the trophic support mediated by these cells can rescue the functional and structural alterations of damaged salivary glands. However, potential differentiation and paracrine effects of hDPSCs in diabetic-induced parotid gland damage have not been investigated. Our study aimed to investigate the therapeutic effects of intravenous transplantation of hDPSCs on parotid gland injury in a rat model of streptozotocin (STZ)-induced type 1 diabetes.Methods: Thirty Sprague–Dawley male rats were randomly categorised into three groups: control, diabetic (STZ), and transplanted (STZ + hDPSCs). The hDPSCs or the vehicles were injected into the rats’ tail veins, 7 days after STZ injection. Fasting blood glucose levels were monitored weekly. A glucose tolerance test was performed, and the parotid gland weight, salivary flow rate, oxidative stress indices, parotid gland histology, and caspase-3, vascular endothelial growth factor, proliferating cell nuclear antigen, neuronal nitric oxide synthase, endothelial nitric oxide synthase, and tetrahydrobiopterin biosynthetic enzyme expression levels in parotid tissues were assessed 28 days post-transplantation.Results: Transplantation of hDPSCs decreased blood glucose, improved parotid gland weight and salivary flow rate, and reduced oxidative stress. The cells migrated to the STZ-injured parotid gland and differentiated into acinar, ductal, and myoepithelial cells. Moreover, hDPSCs downregulated the expression of caspase-3 and upregulated the expression of vascular endothelial growth factor and proliferating cell nuclear antigen, likely exerting pro-angiogenic and anti-apoptotic effects and promoting endogenous regeneration. In addition, the transplanted cells enhanced the parotid nitric oxide-tetrahydrobiopterin pathway.Conclusions: Our results showed that hDPSCs migrated to and survived within the STZ-injured parotid gland, where functional and morphological damage was prevented due to the restoration of normal glucose levels, differentiation into parotid cell populations, and stimulation of paracrine-mediated regeneration. Thus, hDPSCs may have potential in the treatment of diabetes-induced parotid gland injury.

Cerebral small vessel disease (CSVD) is a leading cause of stroke, cognitive impairment, and vascular dementia, yet disease-modifying therapeutic strategies remain limited. Emerging evidence suggests that sleep fragmentation (SF), a common and often under-recognized feature of aging and cardiometabolic disorders, plays a pivotal role in CSVD pathogenesis by disrupting the glymphatic system, the brain’s primary waste clearance pathway. Sleep-dependent glymphatic function facilitates the removal of neurotoxic metabolites and maintains neurovascular homeostasis. In contrast, SF impairs cerebrospinal fluid (CSF)–interstitial fluid (ISF) exchange, promotes perivascular space enlargement, endothelial dysfunction, blood–brain barrier (BBB) breakdown, and chronic neuroinflammation, hallmarks of CSVD. This review synthesizes current mechanistic, preclinical, and clinical evidence linking SF to glymphatic dysfunction and small vessel pathology, framing these interactions as a sleep–glymphatic–vascular continuum underlying CSVD progression and cognitive decline. We further explore the emerging therapeutic potential of tocotrienols (T3), vitamin E isoforms with potent antioxidant, anti-inflammatory, and vasculoprotective properties, as modulators of neurovascular integrity within this continuum. Although direct evidence linking T3 to glymphatic regulation remains limited, converging data support their capacity to preserve endothelial function, attenuate oxidative stress, and stabilize astrocytic and BBB dynamics, mechanisms highly relevant to glymphatic and microvascular health. By integrating sleep biology, glymphatic neuroscience, and nutritional vascular protection, this review highlights hypothesis-generating preventive and therapeutic avenues for CSVD and delineates key knowledge gaps, including the need for longitudinal human studies, standardized glymphatic imaging, objective sleep phenotyping, and interventional trials to establish causal and translational relevance.