Spinal cord injury (SCI) is an unfortunate experience that may generate extensive sensory and motor disabilities due to the destruction and passing of nerve cells. MicroRNAs are small RNA molecules that do not code for proteins but instead serve to regulate protein synthesis by targeting messenger RNA's expression. After SCI, secondary damage like apoptosis, oxidative stress, inflammation, and autophagy occurs, and differentially expressed microRNAs show a function in these procedures. Almost all animal and plant cells release exosomes, which are sophisticated formations of lipid membranes. These exosomes have the capacity to deliver significant materials, such as proteins, RNAs and lipids, to cells in need, regulating their functions and serving as a way of communication. This new method offers a fresh approach to treating spinal cord injury. Obviously, the exosome has the benefit of conveying the transported material across performing regulatory activities and the blood-brain barrier. Among the exosome cargoes, microRNAs, which modulate their mRNA targets, show considerable promise in the pathogenic diagnosis, process, and therapy of SCI. Herein, we describe the roles of microRNAs in SCI. Furthermore, we emphasize the importance of exosomal microRNAs in this disease.
Orthosiphon stamineus Benth, commonly used in Southeast Asia for its medicinal properties, is traditionally employed to treat diabetes and hypertension. Scientific research has validated that O. stamineus extract exhibits significant vasodilatory action on rat aorta. This effect is primarily due to the synergistic interaction among key compounds: eupatorin, sinensetin and 3'-hydroxy-5,6,7,4'-tetramethoxyflavone (TMF). Our previous publication identified the optimum formulation, G28, which contains eupatorin, sinensetin and TMF in the ratio of EC20:EC15:EC5. Therefore, the aim of this study was to investigate the antihypertensive effect and mechanism of action of formulation G28. In this study, aortic rings from spontaneously hypertensive rats (SHRs) and Sprague-Dawley (SD) rats were used to examine the vasodilation mechanisms. The antihypertensive effect of G28 was also assessed through repeated-dose administration in SHRs. G28 exhibited stronger vasorelaxant effects in SHR versus SD rat aortic rings, indicating higher potency under hypertensive conditions. The effect was partially endothelium-dependent, as endothelium removal reduced responses in both aortic rings. G28 retained efficacy with Nω-Nitro-1-arginine methyl ester, methylene blue and 1H-[1,2,4]Ox-adiazolol[4,3-α]quinoxaline-1-one, suggesting involvement of the NO/sGC/cGMP pathway. Additionally, G28's effect diminished with glibenclamide, barium chloride, 4-aminopyrine and tetraethylammonium, indicating potassium channel involvements. The vasorelaxant effect was not significantly altered by indomethacin, atropine, or propranolol (in SD rats only), suggesting independence from the cyclooxygenase, beta-adrenergic (in SD rats only) and muscarinic pathways. G28 also reduced intracellular Ca²⁺ in vascular smooth muscle by antagonising voltage-gated calcium channel and Inositol triphosphate receptor. In vivo, G28 significantly reduced blood pressure in SHRs over 21 days of oral administration, underscoring its potential for hypertension control. G28 shows strong antihypertensive effects via NO/sGC/cGMP, potassium and calcium channels. Its sustained blood pressure reduction in SHRs highlights potential as a promising hypertension treatment option.