## 3 Results
The above study showed that curcumin could stimulate the differentiation of oligodendrocyte progenitors, counteracting their maturation arrest induced by TNF-\(\alpha\). The above effects were ascribed to a mechanism implicating PPAR-\(\gamma\)[52]. In addition, curcumin was found to affect phosphate group transfer to kinase 1/2 (ERK1/2), regulating the transition of ancestral oligodendrocytes to immature oligodendrocytes through a partly dependent PPAR pathway [52]. Curcumin was shown to enhance the amounts of PPAR-\(\gamma\) co-activator co-factor-1\(\alpha\), PGC1-\(\alpha\), and cytochrome c oxidase core protein COX1, while oligodendrocyte progenitors were found in the TNF-\(\alpha\) environment via a PPAR-\(\gamma\)-regulated pathway [52]. These data are consistent with the proven PPAR-\(\gamma\) capability to induce mitochondria structure integrity and activities that are essential for the evolutionary maturation of oligodendrocytes. This study supported evidence for the potential beneficial effects of curcumin in demyelinating diseases, which could be ascribed to its neuroprotective activities and its actions against inflammation [52]. [PERSON] et al. investigated whether the bioactive compound carnosic acid from Rosmarinus, which is used in folk medicine, may have a controlling role in the formation and functions of brown adipocytes [53]. In human pluripotent adipose-derived stem cells (hMADS) transformed to white or brown adipose tissue cells, the transcription and translation of critical regulatory genes were identified [53]. Carnosic acid was found to suppress white adipocyte browning and downregulate thermogenic factor gene expression. In particular, the effects of carnosic acid could be fully reversed, while transaction activation assays showed that carnosic acid exhibits PPAR-\(\alpha/\gamma\) antagonistic activity [53]. Wogonin is a major flavonoid found in _Scutellaria radicans_. It has been considered to exert a crucial impact in terms of modulating both the inflammatory and oxidation pathological states. Research by [PERSON] et al. identified novel pathways by which wogonin may enhance phagocytosis in rodent models of cerebral hemorrhage, thereby enhancing the hematoma resolution and neurological recovery after a cerebral hemorrhage [54]. The above effects could be attributed to upregulated expression of MerTK, Axl, LAMP2, and CD3 in peri-hematoma microglial and BV2 cells. In this context, the wogonin treatment of a mouse model of intracerebral hemorrhage induced microglial phagocytosis in vitro [54]. In addition, by suppressing the pro-inflammatory cytokines and pro-oxidant enzymes'production like TNF-\(\alpha\), IL-1\(\beta\), and inducible nitric oxide synthase (iNOS) after intracerebral hemorrhage, wogonin significantly reduced the inflammatory and oxidative stress responses [54]. Remarkably, the wogonin actions were reversed by GW9662, a PPAR-\(\gamma\) inhibitor. Thus, this study provides strong evidence that wogonin may improve hematoma clearance and neurobehavioral regaining with the aid of PPAR-\(\gamma\)[54]. Butain, a flavonoid analog, naturally found in _Faba bean_, has demonstrated glucose-regulating properties in diabetic patients. An in silico analysis further confirmed that butain may exert a significant impact in glycemic control by regulating PPAR-\(\gamma\) activity. On the basis of this evidence, the antidiabetic properties of butain were explored in models of diabetes induced in rats. However, lutein as a hydrophobic compound has poor bioavailability [55]. Therefore, a lutein formulation using the biopolymer chitosan was prepared to evaluate its synergistic glucose-lowering effects. Both lutein and a butein-chitosan combination were effective in the regulation of the glucose concentration in blood of rats, whereas there were no observed side effects [55]. In addition, a possible mechanism of butein's antidiabetic effect was revealed by gene expression analysis, which was associated with PPAR-\(\gamma\) suppression.