## 4 Conclusions  
Current evidence supports the deepened exploration of RA as a promising therapeutic agent against a wide variety of modern lifestyle disorders (Table 1). However, mechanisms underlying RA's therapeutic activity need further investigation. Initial studies indicate that RA may act through various mechanisms, such as exerting anti-inflammatory and antioxidant effects as well as inhibiting cell proliferation, migration, and selectively inducing cancer cells apoptosis. In addition, RA's anti-angiogenic effects, as demonstrated through human umbilical vein endothelial cells proliferation, migration, adhesion, and tube formation inhibition, suggest that it can be beneficial in preventing tumor growth and metastasis. Thus, given the above-highlighted aspects, rosmenary extract can be conceived as a rich source of potential candidates to be included in the diet with promising effects at pre-determined doses, avoiding toxicity. \begin{table}
\begin{tabular}{c l c} \hline \hline
**Biocative Effects** & **Mechanisms** & **References** \\ \hline \hline \multirow{7}{*}{Anticancer} & Prevent tumor formation development, reduce lipid peroxidation byproducts and proapoptotic proteins expression & [18] \\ \cline{2-3}  & Cause cell cycle arrest and stimulate MMP dysfunction-activated PARP- cleavage & [20] \\  & Blev6 translocation from cytosol to the nucleus & [23, 24] \\ \cline{2-3}  & Inhibit HL-60 promyelocytic leukemia cells’ growth and development & [21, 24] \\ \cline{2-3}  & Induc apoptosis & [21] \\ \cline{2-3}  & Inhibit transcription factor HI-1a expression & [19] \\ \cline{2-3}  & Promote Nic/I2 translocation from cytoplasm to the nucleus & [19] \\ \cline{2-3}  & Increase MPRZ activity efflux & [25] \\ \cline{2-3}  & Stop tumor formation and proliferation & [25] \\ \cline{2-3}  & Reduce TNF-6, COX-2, IL-6 levels and modulates p65 expression & [31] \\ \cline{2-3}  & Module histone deacetylases expression & [31] \\ \hline \multirow{7}{*}{Antidiabetic} & Increase key genes expression involved in mitochondrial biogenesis like PCC-1a, SIRT-1, and TFAM via AMPK activation & [37] \\ \cline{2-3}  & Decrease serine IRS-phosphorylation and enhance GLUT4 translocation & [38] \\ \cline{2-3}  & Increase GLUT4 expression and decrease PEFCK expression & [39] \\ \cline{2-3}  & Enhance antioxidant defense system & [39] \\ \cline{2-3}  & Reduce blood glucose, advanced glycation end-products, HbA1c, IL1,0, TNFa, IL8, p-JNK, P98 MAPK, and NF-kB & [41] \\ \cline{2-3}  & Reduce FFA, triglycerides, serum cholesterol, AOPs, lipid peroxidides, and protein carbonyls levels & [42] \\ \cline{2-3}  & Presence normal insulin secretion & [42] \\ \cline{2-3}  & Attanate pro-inflammatory T helper 2 and T regulatory cells & [12] \\ \cline{2-3}  & Increase the population of diabetes-resistant bacteria and decrease the number of diabetes-sensitive bacteria & [12] \\ \hline \multirow{7}{*}{Antimicrobial} & Exhibit antibacterial activity against 5, _survas_ & [46] \\ \cline{2-3}  & Suppress MSCAMM’s protein expression in 5, _survas_ & [46] \\ \cline{2-3}  & Exert antimicrobial activity against _Entrobericracao_, lactic acid bacteria, _Pusulonomous spp., psychotropic, yeast, and mold & [50] \\ \cline{2-3}  & Inhibit S. _carnas_ LTH1502 and _E. coli_ K-12 LTD4263 growth & [48] \\ \hline \multirow{7}{*}{Cardioprotective} & Inhibit H/8-induced cardiomyocyte apoptosis and down-regulate the expression of cleaved caspase of p-AKT & [54] \\ \cline{2-3}  & Improve insulin sensitivity, reduce lipid levels and p22 phase subunit of nicotinamide adenine dinucleotide phosphate reduced oxidase expression & [57] \\ \cline{2-3}  & Inhibit PDA, TNF-a, IL-induced EFCK shedding by TACE expression suppression & [55, 56] \\ \cline{2-3}  & Reduce ERK/1, PDA\(\cdot\)stimulated p38 and JNK phosphorylation & [55, 56] \\ \hline \hline \end{tabular}
\end{table} 
Table 1: Bioactive effects of rosmarific acid.