Paeoniflorin inhibits excitatory amino acid agonist-and high-dose morphine-induced nociceptive behavior in mice via modulation of N-methyl-D-aspartate receptors.

BACKGROUND: Pain, the most common reasons for physician consultation, is a major symptom in many medical conditions that can significantly interfere with a person's life quality and general functioning. Almost all painkillers have its untoward effects. Therefore, seeking for a safe medication for pain relieve is notable nowadays. Paeonia lactiflora is a well-known traditional Chinese medicine. Paeoniflorin is an active component found in Paeonia lactiflora, which has been reported to inhibit formalin-induced nociceptive behavior in mice. Aims of this present study were to investigate effects of paeoniflorin on excitatory amino acid agonist- or high-dose morphine-induced nociceptive behaviors in mice. RESULTS: Paeoniflorin (100, 200, 500 nmol, i.c.v.) alone and combined with glutamatergic antagonists (MK-801 14.8 pmol, or NBQX 5 nmol, i.t.) inhibited nociception. Those agents also inhibited the clonic seizure-like excitation induced by high-dose morphine (250 nmol, i.t) in mice. Antisense oligodeoxynucleotides of NMDA receptor subunits NR1, NR2A, NR2B significantly enhanced the inhibition of paeoniflorin on excitatory amino acid-and high-dose morphine-induced nociception. Docking energy data revealed that paeoniflorin had stronger binding activity in NR2A and NR2B than NR2C of NMDA receptors. CONCLUSIONS: Results of this study indicate that paeoniflorin-induced inhibition of excitatory amino acid agonist- and high-dose morphine-induced nociceptive behaviors might be due to modulation of NMDA receptors, specifically the NR2B subunit.

[Dysmenorrhea: a study of affected factors and approaches to relief among female students at a college in southern Taiwan].

BACKGROUND: Dysmenorrhea is a major problem in the general gynecology clinic. It causes discomfort among healthcare staffs and significant losses in terms of time and finances. PURPOSE: The purpose of this study was to determine the affected factors of dysmenorrhea and evaluate the self-perceived efficacy of relief methods. METHODS: A cross-sectional research design was used to collect data. Participants included 586 female students enrolled at a college in southern Taiwan. Data was analyzed using a t-test, one-way ANOVA, and Scheffe test. RESULTS: Traditional Chinese medicine pattern identifications related significantly to dysmenorrhea frequency perception. Lifestyle characteristics related significantly to dysmenorrhea level perception. Using shenghua decoction, siwu and pig blood decoction, Angelica drink, ginger, ziziphus jujube, brown sugar tea, and analgesics all related significantly to dysmenorrhea relief efficacy. CONCLUSIONS/IMPLICATIONS FOR PRACTICE: Strategies found to help relieve dysmenorrhea level perception include increasing the duration and regularity of sleep and avoiding the consumption of pungent foods. Seeking and adhering to physician recommendations can also increase dysmenorrhea self-care efficacy. Dysmenorrhea-relief courses should be improved in hospitals and schools to assist women to self-manage dysmenorrhea more effectively.

Post-treatment of Ganoderma lucidum reduced liver fibrosis induced by thioacetamide in mice.

The present study was aimed at assessing the effects of Ganoderma lucidum extract (GLE) on an established liver fibrosis model with reference to the previously reported hepatoprotective effect of GLE against CCl(4)-induced fibrosis in rats. Repeated administration of thioacetamide (TAA) for 12 weeks to mice induced liver fibrosis. Treatment with GLE after the induction of liver fibrosis decreased the hepatic hydroxyproline content and improved liver histology. RT-qPCR analysis showed that GLE treatment reduced the mRNA expression of collagen (alpha1)(I), smooth muscle alpha-actin, tissue inhibitor of metalloproteinase 1 and metalloproteinase-13. In addition, the TAA-induced decrease in total collagenase activity was reversed by GLE treatment. In conclusion, oral administration of GLE reversed TAA-induced liver fibrosis, the mechanism of which might be related to the enhancement of collagenase activity.

Inhibitory effect of olive oil on fibrosis induced by carbon tetrachloride in rat liver.

BACKGROUND & AIMS: In this study, the inhibitory effect of olive oil on liver fibrosis induced by carbon tetrachloride (CCl(4)) has been investigated in rats. METHODS: Rats were divided randomly into four groups: control, CCl(4), and two olive oil groups. Except for rats in the control group, all rats were orally administered CCl(4) twice a week for 8 weeks. Rats in the olive oil groups were treated daily with olive oil (2 or 10 ml/kg) through gastrogavage for the entire experimental period. RESULTS: RT-PCR analysis showed that CCl(4) increased the hepatic mRNA expressions of lipopolysaccharide binding protein, CD14, Toll-like receptor-4, NADPH oxidase, nuclear factor-kappa beta, collagen (alpha1) (I), collagen (alpha1) (III), and transforming growth factor beta1. The expression of these mRNAs could be decreased by olive oil treatment. In addition, Western blot analysis also supported these results. CCl(4)-induced liver damage, as characterized by the increase in hepatic malondialdehyde and hydroxyproline levels. Olive oil treatment decreased the hepatic malondialdehyde and hydroxyproline levels. Histological evaluations showed that olive oil could attenuate the liver fibrosis, necrosis, and expression of smooth muscle alpha-actin that are induced by CCl(4). CONCLUSION: It is speculated that the phenolic compounds in olive oil significantly reduced CCl(4)-induced hepatic fibrosis in rats.

Lipid peroxidation products do not activate hepatic stellate cells.

Lipid peroxidation (LPO) is known to be associated with liver fibrosis in chronic liver injury. However, direct effects of the products of LPO on liver fibrogenesis are still not clear. In this study, we examined the LPO products, such as malondiladehyde (MDA), 8-iso-prostaglandin F(2alpha) (8-iso-PGF(2alpha)), and 15-keto-13,14-dihydro-PGF(2alpha) (15-keto-PGF(2alpha)), on the activation of hepatic stellate cells (HSCs) in vivo and in vitro. Carbon tetrachloride (CCl(4)) was given orally to rats twice a week for 8 weeks. Corn oil was given daily to rats for 8 weeks. CCl(4) induced both free-radical-medicated and cyclooxygenase-2-dependent LPO. Free radical-medicated LPO showed an increase with corn oil treatment, whereas no effect was reflected on COX-2-dependent LPO. CCl(4) induced liver fibrosis in rats, but no liver fibrosis was observed in rats treated with corn oil. In vitro studies demonstrated that MDA, 8-iso-PGF(2alpha) and 15-keto-PGF(2alpha), did not activate HSCs, which were preactivated or not preactivated by TGF-beta1. Our results clearly indicate that LPO products, such as MDA, 8-iso-PGF(2alpha) and 15-keto-PGF(2alpha), cannot directly activate HSCs.

Inhibitory effect of Solanum nigrum on thioacetamide-induced liver fibrosis in mice.

AIM: Solanum nigrum (Solanaceae) has been used in traditional folk medicine for its hepatoprotective agent. The purpose of this study was to investigate the effects of Solanum nigrum extract (SNE) on thioacetamide (TAA)-induced liver fibrosis in mice. MATERIALS AND METHODS: Hepatic fibrosis was produced by TAA (0.2 g/kg, i.p.) three times a week for 12 weeks. Mice in the three TAA groups were treated daily with distilled water and SNE (0.2 or 1.0 g/kg) via gastrogavage throughout the experimental period. RESULTS: SNE reduced the hepatic hydroxyproline and alpha-smooth muscle actin protein levels of TAA-treated mice. SNE inhibited TAA-induced collagene (alpha1)(I) and transforming growth factor-beta1 (TGF-beta1) mRNA levels in the liver. Histological examination also confirmed that SNE reduced the degree of fibrosis caused by TAA treatment. CONCLUSION: Oral administration of SNE significantly reduces TAA-induced hepatic fibrosis in mice, probably through the reduction of TGF-beta1 secretion.

Corn oil enhancing hepatic lipid peroxidation induced by CCl4 does not aggravate liver fibrosis in rats.

UNLABELLED: Lipid peroxidation (LPO) is known to be associated with liver fibrosis in chronic liver injury. However, direct effects of the products of LPO on liver fibrogenesis have not been demonstrated. In this study, we examined the LPO products of carbon tetrachloride (CCl4)+corn oil to evaluate the effect of LPO products on liver fibrosis. CCl4 was given twice a week for 8 weeks. Corn oil was given daily to rats at a dose of 2 or 10ml/kg via gastrogavage throughout the whole experiment period. CCl4 induced both cyclooxygenase (COX)-2 independent and COX-2 dependent LPO. COX-2 independent LPO was enhanced by corn oil treatment while no effect was reflected on COX-2 dependent LPO. CCl4-induced liver fibrosis in rats was not aggravated by corn oil treatment. In addition, the amount of fatty liver induced by CCl4 was increased by corn oil treatment. Though the inflammation-related UCP-2 mRNA expression was induced by CCl4, it was not aggravated by the enhancement of corn oil. CONCLUSION: corn oil enriches polyunsaturated fatty acids through COX-2 independent pathways to increase LPO products that do not enhance liver fibrosis induced by CCl4.

Further studies on the hepatoprotective effects of Anoectochilus formosanus.

The purpose of this study was to investigate the hepatoprotective effects of Anoectochilus formosanus effective fraction (AFEF) on chronic liver damage induced by carbon tetrachloride (CCl4) in mice. CCl4 (5%; 0.1 mL/10 g body weight) was given twice a week for 9 weeks, and mice received AFEF throughout the whole experimental period. Plasma GPT, hepatic levels of hydroxyproline and malondialdehyde were significantly lower in mice treated with AFEF compared with those treated with CCl4 only. Liver pathology in the AFEF-treated mice was also improved. RT-PCR analysis showed that AFEF treatment increased the expression of methionine adenosyltransferase 1A and decreased the expression of collagen(alpha1)(I) and transforming growth factor-beta1. These results clearly demonstrated that AFEF reduced the hepatic damage induced by CCl4 in mice.

Treatment of chronic liver injuries in mice by oral administration of ethanolic extract of the fruit of Hovenia dulcis.

The present study examined the effects of an ethanolic extract of the fruit of Hovenia dulcis (EHD) on chronic hepatitis induced by carbon tetrachloride (CCl(4)) in mice. CCl(4) (5%; 0.1 ml/10 g body weight) was given twice a week for 9 weeks, and mice received EHD throughout the entire experimental period. Plasma activities of GPT and GOT, and hepatic levels of malondialdehyde were significantly lowered in mice treated with EHD as compared to mice treated with CCl(4) only. Histological evaluation showed that EHD could attenuate the liver fibrosis and necrosis caused by CCl(4). RT-qPCR analysis also showed that EHD treatment decreased hepatic collagen (alpha1)(I) and collagen (alpha1)(III) mRNA expressions. Chronic CCl(4) treatment caused liver injuries in mice, characterized by an increase in hepatic methionine adenosyltransferase (MAT) 2A gene expression, and decreased MAT1A gene expression. EHD significantly reduced the changes in MAT gene expression due to the chronic CCl(4) treatment. These results clearly demonstrate that the EHD can reduce hepatic injuries in mice induced by CCl(4).