## 4 Discussion
Biodegradable polymers degrade naturally within the body and release drugs at a constant rate [47]. The PLGA copolymer undergoes degradation by hydrolysis; as the water penetrates the polymer matrix, it disrupts the van der Waals forces and hydrogen bonds and causes cleavage of covalent bonds, thereby leading to degradation. Constant degradation occurs as the carboxylic end group autocatalyzes the degradation process. As water penetrates into the matrix, it hydrolyzes the PLGA copolymer into oligomeric and monomeric products. The encapsulated contents will be released by diffusion until the polymer is solubilized completely [48]. The study conducted on the release study was the proof-of-concept for the encapsulation of geranilin. As it was a combination of PEG and PLGA; therefore, the erosion would be different from PLGA only. Here, the results of our study supported the findings reported by [PERSON] et al. (2017) [49], who reported that a hydrophilic drug encapsulated in PEG-b-PLGA NPs exhibited a biphasic drug release pattern. Thus, the biphasic drug release pattern appears to be common among encapsulated polymeric NPs. Particle toxicity is also a concern in phytochemical and drug discovery. The cell viability test using MTT was employed to assess the percentage of viable cells after treatment with NPs. The highest percentage of viability was observed at the concentration of 1 \(\upmu\)g/mL for both PEG-b-PLGA NPs and PEG-b-PLGA NPs encapsulated with geranilin. At the highest concentration (50 \(\upmu\)g/mL), more than half (50%) of the cells were still viable for both groups. These results suggest that PEG-b-PLGA NPs are biodegradable, which may help overcome undesirable toxicity. PLGA polymers degrade into the biocompatible metabolites lactic acid and glycolic acid by hydrolysis [50]. The lactic acid is small enough to enter into the cells via the monocarboxylate transporter. It serves as an ab energy substrate and free radical scavenger for the cells. Research suggests that damage caused by free radicals leads to cell death [51]. Therefore, lactic acid prevents the cell from being damaged. In addition, lactic acid can promote cell proliferation [52]. Moreover, another study suggested that glycolic acid can induce cell proliferation [53]. Glycolic acid is an alpha-hydroxy acid that naturally occurs in sugarcane, and it is one of the components in PEG-b-PLGA that does not affect the normal functions of the cells. PEG also is widely known to be non-reactive and safe to biological cells [54; 55]. [PERSON] et al. (2012) [56] reported that PEG used as a surfactant in the formulation of a herbicide exhibited no cellular toxicity, even at high concentrations of 100 mM. Generally, PEG appears to have low toxicity to cells except at very high doses. Low toxicity of PEG may be due to the methoxy capping of PEG [57]. Additionally, [PERSON] et al. (2001) [58] reported that PEG showed potent cancer chemopre activity, as it exhibited a dose-dependent inhibitory effect on colon cancer cell growth without any significant toxic effect on the normal colon cell line. These findings provide a reasonable explanation for the non-toxic effect of different concentrations of PEG-b-PLGA NPs on cell viability. Even at the highest concentration of geranilin-encapsulated NPs (50 \(\upmu\)g/mL), cell viability was 61.9%, which means that there was no median lethal dose for the doses tested. Geranilin is a plant compound that has antioxidant properties and is capable of scavenging reactive oxygen species [59]. The functional hydroxyl group, in its structure, mediates the antioxidant effects. However, there was a drop in the percentage of cell viability when cells were treated with geranilin-encapsulated NPs compared to those treated with blank NPs. This could be due to the higher molecular weight of geranilin (952.648 g/mol), which, together with its bulky molecules, might pose a steric hindrance to the donation of the phenolic hydrogen of the hydroxyl group to free radicals.