200 μM: HE49 cells, increase in RLS by 8.5 PD (20%) and 7.1 PD (2% O2); NYaKe cells, increase in RLS by 3.5 PD; WS3RGB cells, increase in RLS by 5.5 PD
Reduction of the rate of telomere shortening; decreased ROS level under 20% oxygen but not under 2% oxygen
2BS and WI38 fibroblasts; 0.3125 μg/ml: no effect on RLS reported
Enhanced proliferation of cells during seven days of incubation. 3.5% SA-β-gal-positive cells seen in PD30 2BS cells, vs. 60% in late PDL cells; in berberine-treated 2BS cells (PD45), the SA-β-gal-positive cell rate reverted to 16%, as compared to the control group (56.5%). Decreased level of p16; cyclin protein and cyclin-dependent kinases, such as cyclin D1 and CDK4 increased. Upregulated level of phosphorylated retinoblastoma protein (pRB)
HFF1 cells; 20 mM: RLS increased by 7.4 and 9.4 PD; 30 mM: RLS increased by 3.0, 4.3 and 6.3 PD; 50 mM: RLS decreased. MRC-5 cells; 20 mM: RLS extension by 10 and 14 PD; 30 mM: RLS extension by 4 and 8 PD; 20 mM and 30 mM, introduced at 55 PD: RLS increase by 13.0 and 12.1 PD, respectively. HFF-1 cells; 20 mM D-carnosine: no effect
50 mM carnosine: more flat, spread-out appearance; maintaining nonsenescent morphology
Human diploid fibroblasts (HDFs); no effect of RLS reported
Young HDFs: reduced expression of SOD1, CAT, and CCS. Senescent cells: increased expression of the SOD2 and MAPK14 genes, downregulation of TP53 gene expression. Young and senescent HDFs: decreased expression of CDKN2A gene, increased expression of MAPK14 gene
WI-38 cells; concentration not specified: increase of RLS (from 64 to 68 when added at 26 PD, from 62 to 65 when added at 42 PD, and from 62 to 63 when added at 58 PD)
Human diploid fibroblasts (HDF); 12.5 μM: effect on RLS not reported
Decrease of ROS level, increased mitochondrial potential, more intact mitochondrial DNA, elevated activities of antioxidative enzymes, more juvenile cell status
HDFs maintained until different passages: PD 8-12 (young cells) and PD 34-36 (senescent cells). Senescent HDFs starved with serum-free DMEM overnight and then incubated in DMEM containing 10 or 30 μM Rg3(S) or (R) for 48 h: no effect on RLS reported
Decrease in percentages of SA-β-gal staining cells in replicatively old HDFs. Reversal of the replicative senescence of HDFs: restoration of the ATP level and NAD+/NADH ratio in senescent HDFs. Recovering the cellular levels of ROS and the NAD+/NADH ratio in young HDFs treated with rotenone. Downregulation of phosphatidylinositol 3-kinase/Akt through the inhibition of mTOR by cell cycle regulators like p53/p21 in senescent HDFs. Activation of sirtuin 3/PGC1α to stimulate mitochondrial biogenesis. Rg3(R) did not alter the corresponding signaling pathways
WI-38 cells; concentration not specified: increase of RLS (from 64 to 67 when added at 26 PD, from 62 to 66 when added at 42 PD, and from 62 to 63 when added at 58 PD)
Primary HDFs derived from foreskins of three different male subjects aged between 9 and 12 years after circumcision; 0.4 mg/ml: no effect on RLS reported
Improvement of cell proliferation of young (143%), presenescent (127.3%) and senescent (157.3%) HDFs. Increased expressions of PRDX6, TP53, CDKN2A, PAK2, and MAPK14 in senescent HDFs. Modulation of the transcriptional profile changes in senescent HDFs. Increased expressions of SOD1, decreased expression of GPX1, PRDX6, TP53, CDKN2A, PAK2, and MAPK14 in PB-treated senescent HDFs
HFL1 fibroblasts; concentration not specified (≤5 μg/ml): a statistically significant increase in RLS, less than 5%
Maintenance of young morphology, delay in appearance of senescent phenotype, increase in growth rate; proteasome activation; morphological rejuvenation
Human dermal fibroblasts; no effect of RLS reported
Significantly increased type I collagen expression and reduced matrix metalloproteinase 1 (MMP-1) expression; reduced intracellular ROS, partially due to activation of the Nrf2-mediated antioxidative response. 50 μM: changes in cell morphology and inhibition in cell proliferation, due to cell cycle arrest in G2/M phase. SA-β-gal and γH2AX unaltered
HEFs; extension of RLS by 2 PD (2 μM), 6 PD (20 μM), and 11 PD (200)
Decreased SA-β-gal staining, decreased ROS level, increase in aconitase activity, decrease in of p53, phospho-p53 at Ser15and p21 and apurinic/apyrimidinic site level, relieve of senescence-related G1 arrest