## 3 Results
assessed the possible effects of pelargonidin against obesity via the suppression of adipogenesis in 3T3-L1 cells [59]. More to the point, pelargonidin was particularly found to decrease 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase (HMG-CoA reductase) LPL, glucose transporter 4 (GLUT4), and adipocyte fatty acid binding protein (A-FABP) expression [59]. Notably, the luciferase reporter assay showed that pelargonidin reduced PPAR-\(\gamma\) transcription action. The above evidence supported that pelargonidin may exert anti-adipogenic activity in 3T3-L1 cells via PPAR-\(\gamma\) suppression. Taken together, the above evidence supported that, through the downregulation of the PPAR-\(\gamma\) signaling pathway, pelargonidin may exhibit anti-adipogenesis activities in 3T3-L1 cells [59]. Moreover, a study investigated if magnolol, a naturally occurring neolignane molecule, may act against [PERSON]'s disease stimulated through beta-amyloid (A\(\beta\)), also exploring the potential mechanisms of its action [60]. Indeed, it has been shown that magnolol reduced A\(\beta\) accumulation, toxicity, and A\(\beta\)-induced memory loss in transgenic _C. elegans_ in a dose-dependent manner [60]. Notably, the above actions were negated by GW9662, a well-known PPAR-\(\gamma\) antagonist. Thus, magnolol appears to mitigate A\(\beta\)-stimulated Alzheimer's disease, and its potential mechanisms may be related to reducing inflammation and promoting PPAR-\(\gamma\)-dependent phagocytosis and A\(\beta\) degradation [60]. Another study explored whether _Malva parciflora_ hydroalcoholic leaf extracts (MpHEs) may act as an anti-inflammatory agent on [PERSON]'s disease progression in lean and obese transgenic 5 XFAD mice [61]. MpHE was found to effectively reduce astrogliosis, the accumulation of insoluble A\(\beta\) peptides in the hippocampus, and spatial learning deficits in both animal groups. These effects have been associated with the accumulation of microglial cells that were close to A\(\beta\) plaques in the cerebral cortex and hippocampus, and with a reduction in several inflammation-related biomarkers [61]. MpHEs, including oleanolic acid and scopoletin, also preserved the phagocytic capacity of microglia through a PPAR-\(\gamma\)/CD36-related manner. In light of the above data, _M. parviflora_ appears to inhibit neuronal inflammation by attenuating the pro-inflammatory M1 phenotype of microglia and enhancing microglial phagocytosis [61]. Hence, _M. parviflora_ could be considered as an alternative agent for preventing mental loss related to metabolism dysfunction, and [PERSON]'s disease development [61]. Recently, renal fibrosis has been found to be attenuated by asiatic acid, a triterpenenoic molecule isolated by the _Centella asiatica_[50]. In this context, the unilateral ureteral occlusion (UUO) model was applied for exploring the mechanisms implicated in the antifibrotic effect of asiatic acid. UUO surgery was performed on Sprague-Dawley rats and mice [62]. Before surgery, the rats were treated with asiatic acid for one week, while the mice were treated with asiatic acid for three days [62]. The UUO group showed a noteworthy extent of kidney damage, interstitial fibrosis, oxidative stress, and stimulation of the transforming growth factor-\(\beta\) (TGF-\(\beta\))/Smad and Wnt/\(\beta\)-catenin signals in the kidney. The pathological changes described above were significantly alleviated through the pre-treatment with asiatic acid. In addition, a co-treatment with GW9662 negated the protective beneficial effects of asiatic acid, highlighting a PPAR-\(\gamma\) dependent action [62]. Although the asiatic acid pre-treatment did not considerably affect the PPAR-\(\gamma\) expression in the kidney, it significantly increased the plasma levels of 15-deoxy-\(\Delta\)12,14-prostaglandin J2 (15d-PGJ2), an endogenous PPAR-\(\gamma\) agonist [62].