## 1 Introduction
### Antioxidant Activity
#### 1.1.2 Antioxidant Activity of Salvia Extracts--In Vitro Cellular and In Vivo Methods
In particular, the oral administration for one month of a methanolic extract of _Salvia salenatica_ (0.1 g/kg), caused a significant decrease of malondialdehydedehyde (MDA) and hydroperoxide levels, in liver and kidney of rats with alcohol-induced damage [76]. In addition, this intake restored the levels of non-enzymatic antioxidants (GSH, vitamin C, vitamin E) while increasing the activities of antioxidant enzymes (SOD, CAT, GPx and GST) [76]. In research performed by [PERSON] et al. [74] in hepatocytes isolated from rats upon supplementation with _S. officinalis_ ethanolic extract (13.33 mg/ml) for 14 days, a decrease of oxidative DNA damage was registered, based on the comet assay. Regardless of this, the SOD level was not changed; the authors demonstrated that the age extract significantly increased the levels of GSH and GPx, suggesting that the consumption of _S. officinalis_ may potentiate resistance to oxidative stress and afford hepatoprotection [74]. More recently, an _S. officinalis_ decoction was shown to significantly reverse the levels of MDA and H\({}_{2}\)O\({}_{2}\), in gastric and intestinal tissues of ethanol-induced gastric and small bowel-injured rats, after 15 days of oral administration [60]. In this study, treatment with age decoction also significantly counteracted (in a dose-related manner) the decreased activities of enzymatic antioxidants SOD and GPx, and levels of the nonenzymatic antioxidant GSH, which were induced by alcohol administration. Overall, the results indicated that the administration of _S. officinalis_ decoction and sulfasalazine (i.e., a drug used in the treatment of inflammatory bowel disease), alone or in combination, abolished acute ethanolic-induced oxidative stress in the gastric and duodenal mucosa, a fact that the authors attributed to the high amount of phenolic acids and flavonoids in the age extract [60]. Several authors also demonstrated the benefits of _Salvia_ commercial polar extracts towards oxidative-stress related disorders. In a study performed by [PERSON] et al. [73], a commercial extract of _S. officinalis_ was administered orally to a lipopolysaccharide (LPS)-induced experimental inflammation animal model for two days, with the aim of investigating the potential antioxidants of the age as a therapeutic approach in inflammatory diseases [73]. Among the samples evaluated, the authors underlined that the extract of _S. officinalis_ (10 and 30 mg/kg) could increase the levels of CAT, SOD, and GPx in the lung, kidney, liver, and erythrocyte hemolysis in treatment groups, and reverse LPS-induced decreases in endogenous antioxidants. Additionally, the age extract used in the treatment groups (inflammation + _S. officinalis_ 10 and 30 mg/kg) decreased the levels of MDA in all samples, and reduced NO levels in the kidney as well, preventing the harmful effects of oxidative stress [73]. Several age plants have also been tested for protective effects on renal disease. In a study performed by [PERSON] et al. [75], a commercial extract of _Salvia prezewalskii_ (SPE) was shown to attenuate oxidative stress in puromycin aminonucleoside (PAN)-induced rat podocyte injury, via antioxidative stress effects--which is reflected by a significant reduction in 8-oxo-2'-deoxyguanosine, a marker of oxidative DNA damage. In the same study, antioxidative stress effects were observed against experimental PAN-induced nephrosis by suppression of ROS levels and podocyte integrity cytoskeleton-restoration, after treatment with SPE. Notably, isolated salvianolic acid B was demonstrated to be as potent as tacrolimus (i.e., a compound that has been used to protect podocytes of glomerular diseases) [75]. The authors also observed significant positive correlations between podocyte apoptosis rates and the ROS levels of groups treated with SPE, as well as the isolated compound salvianolic acid B and rosmarinic acid (r range of 0.998 to 1.0), suggesting that a decrease in intracellular ROS levels may inhibit PAN-induced apoptosis of cultured podocytes [75].