| Introduction: Metronidazole is an extensively used antibiotic and an antiprotozoal medication. Despite its widespread use, little is known about its cardiotoxic effect. Recent studies have raised concerns about its impact on oxidative stress and cardiac tissue integrity. On the other hand, Resveratrol, a plant origin polyphenol, has shown a plethora of beneficial cardiovascular effects. This study was conducted to investigate the prospective prophylactic role of Resveratrol in preventing cardiac muscle toxicity induced by Metronidazole. Material and Methods: Randomly selected 40 adult male albino rats were subdivided into four groups: control, Metronidazole group received 500mg/kg body weight once a day for four weeks by oral administration, Metronidazole + Resveratrol group received Resveratrol first orally using 20mg/kg then Metronidazole orally about 2 hours after administration of Resveratrol for 4 weeks, and Resveratrol group received it for 4 weeks. The cardiac muscle was analyzed using both light microscope as well as transmission electron microscope (TEM). Colorimetric study is used to assess the oxidative stress markers; the malondialdehyde (MDA) and superoxide dismutase (SOD) level in the cardiac muscle tissue. Results: In Metronidazole- administered group, the cardiac MDA level was considerably elevated, the cardiac SOD level was significantly diminished and the histomorphometry of the cardiomyocytes showed marked degeneration and disorganization. In contrast, the cardiac muscle of the Metronidazole + Resveratrol group had colorimetric values and cytoarchitecture that were nearly like the control group. Conclusions: Resveratrol significantly mitigated the oxidative stress and structural cardiac damage induced by Metronidazole, suggesting its potential role as a cardioprotective agent. |
Purpose: Retinal and inner ear ribbon synapses are specialized sensory synapses characterized by synaptic ribbons,
electron-dense and protein-rich structures that enable rapid and sustained neurotransmitter release. This review aims to
examine the molecular architecture of ribbon synapses with a particular focus on the potential involvement of Tiam1, a
guanine nucleotide exchange factor implicated in neuronal development and synaptic plasticity.
Methods: A comprehensive review of the available literature was conducted to summarize current knowledge on the
structural organization and molecular components of ribbon synapses. Particular attention was given to studies investigating Tiam1 expression, function, and its possible role in cytoskeletal remodeling and synaptic regulation.
Results: Evidence supports the central role of RIBEYE as the primary structural component of ribbon synapses; however, the regulatory mechanisms governing ribbon formation and function remain incompletely understood. Recent studies suggest a potential contribution of Tiam1 in modulating synaptic organization and function through Rac1 activation
and cytoskeletal regulation, although direct experimental evidence in ribbon synapses is still limited.
Conclusions: Ribbon synapses are critical for sustained neurotransmission in sensory systems, yet their molecular
regulation remains incompletely defined. Tiam1 emerges as a promising candidate molecule that may influence ribbon
synapse function. Future experimental studies are needed to clarify its localization, molecular interactions, and contribution to synaptic organization and plasticity.
The neural crest (NC) is a transient, multipotent cell population that contributes extensively to vertebrate embryogenesis, generating craniofacial structures, peripheral nerves, melanocytes, and cardiovascular elements. While
classically studied in the context of development, increasing evidence demonstrates that NC-derived cells persist into adulthood, where they support tissue
homeostasis, plasticity, and repair. This review synthesizes current insights
into the lifelong impact of the NC, with emphasis on aging, degeneration, and
regeneration. We first outline the developmental origins and lineage diversification of NC cells, highlighting mechanisms that establish long-lived progenitor pools. We then examine how age-related changes in NC-derived tissues,
including craniofacial bone remodeling, pigmentary alterations, autonomic
decline, and peripheral neuropathies, reflect broader principles of cellular
senescence and disrupted signaling. The involvement of NC derivatives in ageassociated pathologies, such as neurodegeneration, cardiac anomalies, and craniofacial degeneration, is also addressed. Finally, we highlight progress in
regenerative medicine that leverages NC-derived stem and progenitor cells,
together with molecular pathways that may rejuvenate their function in aging
tissues. By integrating developmental, pathological, and regenerative perspectives, this review positions the NC as a central contributor to organismal aging
and underscores its translational relevance. We also outline unresolved questions and future research directions at the interface of NC biology, aging, and
regenerative medicine.
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