## 1 Introduction  
Mesenchymal stem cells (MSCs) and multipotent progenitor cells, which can differentiate into diverse cell types, are promising cell sources for regenerative medicine, tissue engineering, and cell therapy techniques [1, 2]. MSCs can be harvested from various tissues, including bone, adipose tissue, umbilical cord, and dental pulp [2, 3, 4, 5, 6]. In addition to their differentiation potential for clinical applications [3], paracrine secretions from these cells influence the surrounding cellular environment [4]. Consequently, both cells themselves and cell-free extracts, such as extracellular particles (e.g., exosomes) and cytokines, have therapeutic potential and have been extensively investigated for medical applications [1, 5]. Generally, allogeneic somatic cell transplantation elicits immune rejection due to major histocompatibility complex (MHC) mismatches [6], whereas stem cells, including MSCs, result in low levels of immunogenicity [2]. allogeneic cell transplantation is a novel approach for cell therapy [1, 5]. However, the proportion of mesenchymal stem cells in vivo is low [7, 8]. Consequently, long-term cultures are often required to obtain sufficient quantities of the desired therapeutic substances [9, 10]. Furthermore, rigorous quality control is a critical consideration in cell preparation [11]. Rat dental pulp stem cells (DPSCs), originating from the neural crest and classified as a type of MSC, can be obtained through in vitro amplification from commonly harvested dental pulp [12; 13]. DPSCs exhibit multiple markers characteristic of mesenchymal stem cells [14]. MSCs from dental pulp are generally designated as stem cells from human exfoliated deciduous teeth (SHEDs), DPSCs, tooth germ progenitor cells (TGPCs), or Dental Follicle Stem Cells (DFSCs), depending on the site of collection [14]. Similarly to other MSCs derived from various tissues, DPSCs demonstrate multipotency to differentiate into diverse cell types, including osteoblasts, chondrocytes, adipocytes, neurons, and vascular endothelial cells [15]. They also exhibit excellent self-renewal, proliferative capability [16], various immune regulatory effects [17], and anti-inflammatory [18] antiapoptotic effects [19]. Consequently, cell therapies have garnered significant attention in bone regenerative medicine, neurological diseases, diabetes, and other pathological conditions [15]. However, preparing a large number of cells for allogeneic transplantation remains a significant bottleneck to their further clinical application in regenerative medicine [20]. Although in vitro passaging increases cell yield, prolonged cell culture is known to induce cell exhaustion [2] and cellular senescence [21]. Cellular senescence is a cell state in which a proliferating cell undergoes stable cell cycle arrest [22] or irreversible cell cycle exist [23]. In contrast to stress-induced premature senescent cells caused by DNA-damaging stresses (reactive oxygen species, UV light, lipopolysaccharideacharide (LPS), etc. ), replicative senescence results from continuous cell division [24; 25]. The concept of cellular senescence, first proposed by [PERSON] in the 1960s, is attributed to the limited proliferative capacity of somatic cells [26]. In vitro amplified cells exhibiting cellular senescence [21] generally demonstrate proliferation arrest [27], flattened cell morphology [28], nuclear enlargement [29], nucleophilic reticulum fusion [30], and mitochondrial dysfunction [31]. p21, p16, senescence-associated \(\beta\)-galactosidases (SA-\(\beta\)-gal), and urokinase-type plasminogen activator receptor (uPAR) are widely utilized as cell senescence markers [22; 31; 32]. p21 and p16 are molecules involved in cell cycle arrest, primarily acting on CDK1/2 and CDK4/6 [22; 33; 34]. SA-\(\beta\)-gal, lysosomal \(\beta\)-galactosidase activity associated with cellular senescence, is a common and widely utilized marker for identifying senescent cells, although other cells such as macrophages also exhibit positive staining [22].