L-Carnitine ameliorates the liver by regulating alpha-SMA, iNOS, HSP90, HIF-1alpha, and RIP1 expressions of CCL4-toxic rats.

OBJECTIVES: Carbon tetrachloride (CCL4) toxicity triggers fibrosis, activating various mechanisms within the cell. We aimed to create damage with CCL4 and investigate the effectiveness of L-carnitine on the mechanisms we identified. MATERIALS AND METHODS: Forty rats were divided into 5 groups with equal number of rats in each group. Group I: Control group, Group II: L-carnitine group, 200 mg/kg L-carnitine twice a week, Group III: CCL4 group, 0.2 ml/100 gr CCL4, IP, dissolved in olive oil 2 times a week during 6 weeks; Group IV: L-carnitine + CCL4 group, 200 mg/kg L-carnitine 24 hr before 0.2 ml/100 g CCL4 application twice a week; Group V: CCL4 + L-carnitine, 200 mg/kg L-carnitine half an hour after 0.2 ml/100 g CCL4 application. The liver was evaluated histologically. Immunohistochemically stained with α-SMA, iNOS, HSP90, HIF-1α, and RIP1. TNF-α, TGF-ß, AST, ALT, ALP, and GGT measurements were evaluated. RESULTS: In the classical lobule periphery, an increase in lipid accumulation and a decrease in glycogen accumulation were observed. After immunohistochemical measurements and biochemical analyzes, an increase in the expression density of all proteins was observed in group III. In group IV and V, an improvement in tissue and a decrease in protein expression densities were observed. CONCLUSION: iNOS serves as a free radical scavenger in response to damage caused by increased toxicity of α-SMA, HSP90, and HIF-1α. Especially, increased RIP1 level in the tissue indicates the presence of necrosis in the tissue after CCL4-toxicity. Supplementing the amount of endogenous L-carnitine with supplementation provides a significant improvement in the tissue.

The effect of erythropoietin and umbilical cord-derived mesenchymal stem cells on nerve regeneration in rats with sciatic nerve injury.

OBJECTIVE: We aimed to investigate the effects of umbilical cord-derived mesenchymal stem cells and erythropoietin on nerve regeneration in the sciatic nerve 'crush injury' in a rat model. METHODS: Experimental animals were randomly divided into 5 groups: Crush Injury, Sham, Crush Injury + Erythropoietin, Crush Injury + Mesenchymal Stem Cell, Crush Injury + Erythropoietin + Mesenchymal Stem Cell groups. Crush injury made with bulldog clamp. Mesencyhmal stem cells delivered by enjection locally. Erythropoietin administered by intraperitoneally. On the 0th, 14th and 28th days, all groups underwent a sciatic functional index test. On 28th day, sciatic nerves were harvested and histopathological appearance, axon number and axon diameter of the sciatic nerves were evaluated with Oil Red O staining. Immunoreactivity of nerve growth factor, neurofilament-H and caspase-3 were determined by immunofluorescence staining in nerve tissue. RESULTS: In histopathological examination, axons and nerve bundles exhibiting normal nerve architecture in the Sham group. Crush Injury + Mesenchymal Stem Cell group has similar histological appearance to the Sham group. The number of axons were higher in the Mesenchymal Stem Cell groups compared to the Crush Injury group. Nerve growth factor immunoreactivity intensity was significantly lower in Crush Injury + Mesenchymal Stem Cell group compared to Crush Injury group. Neurofilament-H density was higher in the treatment groups when compared to the Crush Injury group. CONCLUSIONS: In this study, it was found that umbilical cord-derived mesenchymal stem cells and erythropoietin treatments effects positively regeneration of crush injury caused by bulldog clamp in the sciatic nerve of rats.

Protective effects of curcumin and beta-carotene on cisplatin-induced cardiotoxicity: An experimental rat model.

OBJECTIVE: Cisplatin (CDDP) has been known to be an effective antineoplastic drug; however, it has a cardiotoxic effect. Curcumin (CMN) and beta-carotene (BC) have been suggested to protect biological systems against CDDP-induced damage. The current study was conducted to evaluate the possible protective roles of CMN and BC on CDDP-induced cardiotoxicity in rat cardiac tissues. METHODS: A total of 49 adult female Wistar albino rats were equally divided into seven groups as follows: control (no medication), sesame oil (1 mg/kg), CDDP (single dose injection two times as once a week, 5 mg/kg/week), BC (100 mg/kg), CDDP+BC (pretreated BC for 30 min before CDDP injection), CMN (200 mg/kg), and CDDP+CMN (pretreated CMN for 30 min before CDDP injection). These treatments were applied intraperitoneally for CDDP and with gavage for CMN and BC. The oxidative/antioxidant indicators, inflammatory cytokines, and histopathological alterations were examined. RESULTS: These alterations included a marked increase in malondialdehyde (MDA) level, significant decrease in catalase (CAT) and superoxide dismutase (SOD) activities, and significant elevation of tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, interleukin (IL)-6 in the CDDP group compared with the other groups. Histopathologically, CDDP-induced severe myocardial degenerative changes were observed. However, the CDDP-induced disturbances in the above-mentioned parameters significantly improved by treatment with BC and particularly CMN. CONCLUSION: This study indicated that CDDP treatment markedly caused cardiotoxicity; however, treatment with CMN or BC ameliorated this cardiotoxicity in rats. Furthermore, these findings revealed that treatment with CMN has a higher cardioprotective effect than that with BC against CDDP-induced cardiotoxicity in rat cardiac tissues.