Carvacrol Exerts Anti-Inflammatory, Anti-Oxidative Stress and Hepatoprotective Effects Against Diclofenac-Induced Liver Injury in Male Rats.

Background: Diclofenac (DIC) is an NSAID that can cause toxic effects in animals and humans and carvacrol (CAR) is a monoterpene compound that displays effective pharmacological and biological actions. The purpose of this work was to assess the influences of CAR on DIC-induced liver injury and oxidative stress in male rats. Methods: The male Wistar rats were segregated into four groups. Group 1, the control group; Group 2 received DIC-only (10 mg/kg BW, p.o); Group 3, received CAR-only (10 mg/kg BW, p.o), and group 4 received DIC plus CAR. The serum levels as well as the activity of several liver-associated markers, and oxidative and anti-oxidant compounds were tested. The expression of pro-inflammatory mediators was also studied using the qRT-PCR analysis. Results: Our results showed that DIC treatment was associated with the elevation in the serum levels of liver-related markers together with the increase in the serum and the hepatic levels of malondialdehyde (MDA) and protein carbonyl (PC). Moreover, DIC reduced the activity of the antioxidant system in the rats and increased lymphocyte infiltration into the hepatocytes. CAR; however, protected the hepatocytes from the toxic effects of DIC by enhancing the activity of antioxidant enzymes such as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and Glutathione (GSH). By diminishing the expression of tumor necrosis factor (TNF)-α, CAR was also capable of preventing the inflammatory effects of DIC on liver cells. Conclusions: The findings of this study indicated that the administration of CAR could alleviate the noxious effects of DIC on the antioxidant defense system and liver tissue.

Carvacrol exerts nephroprotective effect in rat model of diclofenac-induced renal injury through regulation of oxidative stress and suppression of inflammatory response.

Diclofenac (DIC) is an NSAID that can cause toxic effects in animals and humans and carvacrol (CAR) is a monoterpene compound that displays effective pharmacological and biological actions. The purpose of this work was to assess the influences of CAR on DIC-induced renal injury and oxidative stress in male rats. The rats were segregated into four groups. Group 1, control group; Group 2 received DIC-only; Groups 3, received CAR-only and group 4 received DIC plus CAR. Changes in biochemical indexes, pathological changes, molecular biological indexes, and genes related to the inflammation of main organs were evaluated. The results of this work indicated that the amounts of the serum protein carbonyl, sGOT, sGPT, urea, creatinine, uric acid, nitrite content, MDA, serum TNF-α, and renal TNF-α gene expression were remarkably increased and the levels of the GPx, GSH, CAT, and SOD were significantly reduced in DIC-only treated animals compared to the control group. On the other hand, treatment with CAR after exposure to DIC led to significant improvements in abnormalities of DIC-induced renal injury and serum biochemical factors. The data approve that CAR diminished the deleterious effects of DIC exposure. In this regard, the findings of this study indicated that the administration of CAR could alleviate the noxious effects of DIC on the antioxidant defense system and renal tissue.

Human platelet lysate versus minoxidil stimulates hair growth by activating anagen promoting signaling pathways.

Minoxidil and human platelet lysate (HPL) are commonly used to treat patients with hair loss. However, the roles of HPL versus minoxidil in hair follicle biology largely remain unknown. Here, we hypothesized that bulge and dermal papilla (DP) cells may express specific genes, including Kras, Erk, Akt, Shh and ß-catenin after exposure to minoxidil or HPL. The mouse hair follicles were isolated on day 10 after depilation and bulge or DP regions were dissected. The bulge and DP cells were cultured for 14days in DMEM/F12 medium. Then, the cells were treated with 100µM minoxidil and 10% HPL for 10 days. Nuclear morphology was identified using DAPi staining. Reverse transcriptase and real-time polymerase chain reaction (PCR) analysis were also performed to examine the expression of Kras, Erk, Akt, Shh and ß-catenin mRNA levels in the treated bulge and DP regions after organ culture. Here, we found that minoxidil influences bulge and DP cell survival (P<0.05). Apoptosis in DP cells was also meaningfully decreased by HPL treatment (P=0.014). In addition, Kras, Akt, Erk, Shh and ß-catenin mRNA levels were changed in response to minoxidil treatment in both bulge and DP cells. HPL mediated Erk upregulation in both bulge and DP cells (P<0.05), but Kras and Akt mRNA levels were not considerably different in the HPL-treated cells. ß-catenin mRNA level was also significantly increased in the bulge region by HPL. We also found that Shh mRNA level was considerably higher in HPL-treated bulge cells than in minoxidil-treated bulge cells. In contrast, the expression of ß-cateinin and Shh in the DP cells was not meaningfully increased after treatment with HPL. Our results suggest that minoxidil and HPL can promote hair growth by activating the main anagen inducing signaling pathways.