Rosmarinic acid (RA) is a natural polyphenolic compound derived from many common herbal plants. Although it is known that RA has many important biological activities, its effect on proteasome inhibitor-induced changes in cancer treatment or its effects on any experimental proteasome inhibition model is unknown. The aim of the study was to investigate the effect of RA on MG132-induced cytotoxicity, proteasome inhibition, autophagy, cellular stresses, and apoptosis in HepG2 cells. HepG2 cells were treated with 10, 100, and 1000 µM RA in the presence of MG132 for 24 h; 10 and 100 µM RA did not affect but 1000 µM RA decreased cell viability in HepG2 cells. MG132 caused a significant decrease in cell viability and phosphorylation of mammalian target of rapamycin and a significant increase in levels of polyubiquitinated protein, microtubule-associated proteins 1A/1B light chain 3B-II (LC3B-II), heat shock protein 70 (HSP70), binding immunoglobulin protein (BiP), activating transcription factor 4 (ATF4), protein carbonyl, and cleaved poly(adenosine diphosphate-ribose) polymerase 1 (PARP1); 10 and 100 µM RA did not significantly change these effects of MG132 in HepG2 cells; 1000 µM RA caused a significant decrease in cell viability and a significant increase in polyubiquitinated protein, LC3B-II, HSP70, BiP, ATF4, protein carbonyl, and cleaved PARP1 levels in MG132-treated cells. Our study showed that only 1000 µM RA increased MG132-induced cytotoxicity, proteasome inhibition, autophagy, cellular stresses, and apoptosis in HepG2 cells. According to our results, cytotoxic concentration of RA can potentiate the effects of MG132 in hepatocellular carcinoma treatment.

The aim of the present study was to investigate the effect of streptozotocin-induced diabetes mellitus and lipoic acid treatment on serum paraoxonase-1 and paraoxonase-3 protein levels and paraoxonase, arylesterase and lactonase activities.36 rats were equally and randomly divided into 4 groups as control, lipoic acid, diabetes and diabetes+lipoic acid. To induce diabetes, a single dose of streptozotocin (40 mg/kg) was injected intraperitoneally to diabetes and diabetes+lipoic acid groups. Lipoic acid (10 mg/kg/day) was injected intraperitoneally for 14 days to lipoic acid and diabetes+lipoic acid groups. Serum PON1 and PON3 protein levels were measured by western blotting. Serum paraoxonase, arylesterase and lactonase activities were determined by the measuring initial rate of substrate (paraoxon, phenylacetate and dihydrocoumarin) hydrolysis.Streptozotocin-induced diabetes mellitus caused a significant decrease whereas lipoic acid treatment caused a significant increase in serum PON1 and PON3 protein levels and paraoxonase, arylesterase and lactonase activities. The increase percent of serum PON3 protein was higher than that of serum PON1 protein and the increase percent of serum lactonase activity was higher than that of serum paraoxonase and arylesterase activities in diabetes+lipoic acid group.We can report that, like PON1 protein, PON3 protein and actually its lactonase activity may also have a role as an antioxidant in diabetes mellitus and lipoic acid treatment may be useful for the prevention of the atherosclerotic complications of diabetes by increasing serum PON1 and PON3 protein levels and serum enzyme activities.

The fibrinogen to albumin ratio is significantly associated with ischemic RVO. Instead of complicated and invasive methods, such as a retinal angiogram, the fibrinogen to albumin ratio could be a useful initial diagnostic test to predict ischemia in RVO.

We investigated the effects of quercetin on pathological findings on testicular ischaemia-reperfusion (I/R) injury in rats. Twenty-four male Wistar albino rats were randomly assigned into four groups: Group 1, control (n = 5); Group 2, sham (n = 4); Group 3, I/R (n = 8); and Group 4, I/R + quercetin (n = 7). Bilateral testicular artery and vein were occluded for 1 h, followed by reperfusion in I/R and I/R + quercetin animals. Quercetin (20 mg kg(-1) per day) was administrated once daily by gavage to Group 1 and Group 4, respectively, after reperfusion. At the end of the study, bilateral orchiectomies were performed for histopathologic examination. The tissue damage was evaluated with light microscopy. Normal inter-stitium and seminiferous tubules were observed in control group. In the sham group, rats were seen minimal oedema around the seminiferous tubules and congested vascular structures. In Group 3, oedema, vascular congestion and haemorrhage between seminiferous tubules were observed. In Group 4, histopathologic features were markedly less than Group 3 (P = 0.03). Our study demonstrated that quercetin seems to have a protective effect on testis histopathology in rats with testicular I/R.

Objective: The aim of this study was to investigate the protective effect of L-carnitine against to liver damage caused by lipid peroxidation and oxidative stress in toxic hepatitis induced by acetaminophen. Materials and Methods:Wister-albino male rats were divided into three groups randomly: control, toxic hepatitis, and L-carnitine groups. To introduce a toxic hepatitis, single dose of acetaminophen (300 mg/kg) dissolved in warm saline was given intraperitoneally to toxic hepatitis and L-carnitine groups. A single dose of L-carnitine (500 mg/kg) was given intraperitoneally to L-carnitine group five minutes after introducing to toxic hepatitits. A single dose of warm saline was given intraperitoneally to control group. Results: In toxic hepatitis group, serum alanine and aspartate aminotransferase and plasma and liver malondialdehyde levels were higher whereas plasma Gc-globulin, whole blood and liver glutathione levels, erythrocyte and liver catalase activities and erythrocyte glutathione peroxidase activity were lower as compared to control group. In L-carnitine group, serum alanine and aspartate aminotransferase and plasma and liver malondialdehyde levels were lower whereas whole blood and liver glutathione levels, erythrocyte and liver catalase activities and erythrocyte glutathione peroxidase activity were higher as compared to toxic hepatitis group. There was no significant change between plasma Gc-Globulin levels of these groups. Histopathological changes in toxic hepatitis group were more prominent than those found in L-carnitine group. Conclusion: L-Carnitine has a protective effect against to liver damage caused by lipid peroxidation and oxidative stress in toxic hepatitis induced by acetaminopfen in rats.