Effects of yokukansan and donepezil on learning disturbance and aggressiveness induced by intracerebroventricular injection of amyloid β protein in mice

The effects of yokukansan and donepezil on learning disturbance and aggressiveness were examined in amyloid β protein (Aβ)‐injected mice. Intellicage tests showed that both yokukansan and donepezil ameliorated Aβ‐induced learning disturbance, but the ameliorating effect of donepezil was not enhanced by concomitant administration of yokukansan. On the other hand, a social interaction test showed that Aβ‐induced aggressiveness was ameliorated by yokukansan, but not by donepezil. Co‐administration of both drugs also ameliorated aggressiveness, as did yokukansan alone. In vitro binding assays revealed that yokukansan did not bind to choline receptors or transporters. In vitro enzyme assays revealed that yokukansan did not affect choline acetyltransferase activity or inhibit acetylcholinesterase activity, as did donepezil. These results suggest that yokukansan might ameliorate aggressiveness without interfering with the pharmacological efficacy (antidementia effect) of donepezil and also that concomitant administration of yokukansan might be useful for amelioration of aggressiveness, which was not lessened by donepezil. The difference in the efficacies of both drugs may be due to a difference in their pharmacological mechanisms. Copyright © 2010 John Wiley & Sons, Ltd.     

Protective effect of Morinda citrifolia fruits on β‐amyloid (25–35) induced cognitive dysfunction in mice: An experimental and biochemical study

The neuroprotective effect of an ethyl acetate extract of Morinda citrifolia (Rubiaceae) Linn. fruits (EMC, ethyl acetate extract of Morinda citrifolia) at doses of 200 and 400 mg/kg, p.o. was studied on β‐amyloid (25–35) peptide induced cognitive dysfunction in mice. In the step‐down inhibitory avoidance, EMC exhibited a significant increase in short‐term memory and long‐term memory (p < 0.05). A significant decrease (p < 0.01) in escape latency was noticed in the animals in the water maze. A significant increase (p < 0.01) in alteration of behavior was exhibited upon administration of EMC 200 and 400 mg/kg on the Y maze. Exploratory parameters such as line crossings, head dipping and rearing were increased significantly in EMC treated groups in a dose‐dependent manner (p < 0.05 and p < 0.01). A significant reduction (p < 0.05) in acetyl cholinesterase activity was noticed in the EMC 200 and 400 mg/kg treated groups. The level of monoamine oxidase‐A was decreased by the administration of EMC 200 and 400 mg/kg (p < 0.05 and p < 0.01, respectively). EMC at a dose of 400 mg/kg exhibited a significant increase (p < 0.01) in the levels of serotonin and dopamine. Antioxidant enzymes such as superoxide dismutase, glutathione reductase, glutathione peroxidase and ascorbic acid were decreased significantly in the b‐amyloid peptide injected group, whose levels were restored significantly (p < 0.01) by the administration of EMC (400 mg/kg). Copyright © 2009 John Wiley & Sons, Ltd.     

Silibinin protects rat pancreatic β‐cell through up‐regulation of estrogen receptors' signaling against amylin‐ or Aβ1–42‐induced reactive oxygen species/reactive nitrogen species generation

Amylin and amyloid‐β (Aβ) were found to induce reactive oxygen species (ROS) and reactive nitrogen species (RNS) in rat pancreatic β‐cell line, INS‐1 cells, leading to cell death. In this study, we report on reciprocal relationship between the expression of estrogen receptors (ERs) α and β (ERα and ERβ) and generation of ROS/RNS in amylin/Aβ_1–42‐treated INS‐1 cells. That is, pharmacological activation of ERs in INS‐1 cells significantly decreases ROS/RNS generation, but blockage of ERs increases ROS/RNS generation. Silibinin is a natural polyphenolic flavonoid isolated from milk thistle with phytoestrogen activities, also known as silybin. Treatment with silibinin down‐regulated ROS/RNS production induced by treatment with amylin/Aβ_1–42 in the cells. Silencing ERs expression with siRNAs targeting ERs showed that the protective effect of silibinin was markedly weakened, indicating that silibinin protection is largely attributed to activation of ERs' signaling. The binding of silibinin to ERs implies that the protective effect of silibinin on amylin/Aβ_1–42‐treated INS‐1 cells owes to down‐regulation of ROS/RNS through the activation of ERs phosphorylation. Amylin and Aβ_1–42 cotreatment enhanced furthermore ROS/RNS generation and cytotoxicity through further down‐regulation of ERs phosphorylation, and this was reversed by silibinin. Silibinin also protects INS‐1 cells from amylin and Aβ_1–42 cotreatment. These results indicate that protective effect of silibinin is mediated by enhancement of ERs phosphorylation that depresses ROS/RNS generation in amylin/Aβ_1–42‐treated INS‐1 cells.     

Withanamides in Withania somnifera fruit protect PC‐12 cells from β‐amyloid responsible for Alzheimer's disease

Alzheimer's disease (AD) is an irreversible neurodegenerative disorder with symptoms of confusion, memory loss, and mood swings. The β‐amyloid peptide, with 39–42 amino acid residues (BAP), plays a significant role in the development of AD. Although there is no cure for AD, it can be managed with available drugs to some degree. Several studies have revealed that natural antioxidants, such as vitamin E, vitamin C and β‐carotene, may help in scavenging free radicals generated during the initiation and progression of this disease. Therefore, there has been considerable interest in plant phytochemicals with antioxidant property as potential agents to prevent the progression of AD. Our earlier investigations of the Withania somnifera fruit afforded lipid peroxidation inhibitory withanamides that are more potent than the commercial antioxidants. In this study, we have tested two major withanamides A (WA) and C (WC) for their ability to protect the PC‐12 cells, rat neuronal cells, from β‐amyloid induced cell damage. The cell death caused by β‐amyloid was negated by withanamide treatment. Molecular modeling studies showed that withanamides A and C uniquely bind to the active motif of β‐amyloid (25–35) and suggest that withanamides have the ability to prevent the fibril formation. Further understanding of the mechanism of action and in vivo efficacy of these withanamides may facilitate its development as a prophylaxis. Copyright © 2009 John Wiley & Sons, Ltd.     

Effects of Ganoderma lucidum on cellular immunocompetence in γ-irradiated mice

We have investigated the effects on mice treated with Ganoderma lucidum (GI) when the whole body was exposed to 400 rad γ-irradiation. The mice were divided into five groups. Group A was the normal control; group B, the experimental control, was treated with GI; group C was the radiation control (RT); group D was treated with RT and GI; group E was treated with GI, RT and GI. The results revealed that the relative spleen weight had increased significantly in groups B and E on day 7 and increased in all experimental groups on day 28 after irradiation. The leukocyte counts decreased obviously in groups C, D and E on day 7, and recovered in groups D and E was faster than that in group C on day 28. The blastogenic response of splenocytes to LPS, Con A and PHA in groups administered GI were higher than that in group C on days 7 and 28. Therefore, GI seemed to assist the recovery of cellular immunocompetence in γ-irradiated mice.     

Studies on possible protective effect of plant derived phenols and the vitamin precursors—β-Carotene and α-tocopherol on 7,12 dimethylbenz (a) anthracene induced tumour initiation events

Our earlier experiments have shown that the plant phenols—hydroxychavicol, eugenol, catechin, curcumin, and the vitamins—β-carotene and α-tocopherol—are potent inhibitors of polycyclic aromatic hydrocarbon (PAH) induced mutagenesis and carcinogenesis. In an attempt to elucidate their mode of action, we studied their effect on mouse skin DNA synthesis following 7,12 dimethylbenzanthracene (DMBA) treatment and ³H-7,12 dimethylbenzanthracene—DNA interaction in vitro (in the presence of mouse skin S9). With the exception of eugenol, all the phenols and vitamins tested inhibited ³H-DMBA-DNA interaction in vitro. In the DNA biosynthesis assay, of the chemopreventive agents tested only β-carotene effectively modulated DMBA suppressed DNA synthesis in the mouse skin. Our results indicate that the assay of DNA biosynthesis is not of predictive value with respect to the chemopreventive effect of a chemical, while assay of carcinogen—DNA interaction shows correlation between the chemopreventive property and the inhibition of the interaction of carcinogen with DNA.     

Neuroprotective effects of Triticum aestivum L. against β‐Amyloid‐induced cell death and memory impairments

β‐Amyloid (Aβ) is a key component of senile plaques, neuropathological hallmarks of Alzheimer's disease (AD) and has been reported to induce cell death via oxidative stress. This study investigated the protective effects of Triticum aestivum L. (TAL) on Aβ‐induced apoptosis in SH‐SY5Y cells and cognitive dysfunctions in Sprague‐Dawley (SD) rats. Cells treated with Aβ exhibited decreased viability and apoptotic features, such as DNA fragmentation, alterations in mitochondria and an increased Bax/Bcl‐2 ratio, which were attenuated by TAL extract (TALE) pretreatment. To elucidate the neuroprotective mechanisms of TALE, the study examined Aβ‐induced oxidative stress and cellular defense. TALE pretreatment suppressed Aβ‐increased intracellular accumulation of reactive oxygen species (ROS) via up‐regulation of glutathione, an essential endogenous antioxidant. To further verify the effect of TALE on memory impairments, Aβ or scopolamine was injected in SD rats and a water maze task conducted as a spatial memory test. Aβ or scopolamine treatment increased the time taken to find the platform during training trials, which was decreased by TALE pretreatment. Furthermore, one of the active components of TALE, total dietary fiber also effectively inhibited Aβ‐induced cytotoxicity and scopolamine‐caused memory deficits. These results suggest that TALE may have preventive and/or therapeutic potential in the management of AD. Copyright © 2009 John Wiley & Sons, Ltd.     

β‐secretase inhibitory effects of furanocoumarins from the root of Angelica dahurica

In the course of screening antidementia agents from natural products, five β‐secretase (BACE1) inhibitors were isolated from the root extract of Angelica dahurica (Umbelliferae). They were identified as furanocoumarins, isoimperatorin (1), imperatorin (2), (+)‐oxypeucedanin (3), (+)‐byakangelicol (4) and (+)‐byakangelicin (5). Among them, compounds 2 and 4 showed significant inhibitory activity against β‐secretase (BACE1) with IC₅₀ values of 91.8 ± 7.5 and 104.9 ± 2.4 μM , respectively. Compounds 1‐5 inhibited BACE1 activity in a dose‐dependent manner. Copyright © 2009 John Wiley & Sons, Ltd.     

Catalpol provides a protective effect on fibrillary Aβ1–42‐induced barrier disruption in an in vitro model of the blood–brain barrier

Excessive amyloid beta (Aβ) deposition in brain is mainly responsible for cell damage and blood–brain barrier (BBB) disruption in Alzheimer's disease (AD). Catalpol, an iridoid glucoside extracted from the root of Rehmannia glutinosa Libosch, has neuroprotective effect against AD. It is unclear whether catalpol has a protective effect on Aβ‐induced BBB leakage. We employed an immortalized endothelial cell line (bEnd.3) and astrocytes co‐culture to mimic a BBB model in vitro and investigated the effect of catalpol on BBB. We found that treatment with catalpol decreased BBB hyperpermeability induced by fibrillar Aβ_1–42. Data from western blotting showed that catalpol prevented fibrillar Aβ_1–42‐induced bEnd.3 cell apoptosis through mitochondria‐dependent and death receptor pathways; decreased the levels of matrix metalloproteinases (MMPs), MMP‐2, MMP‐9, and the receptor for advanced glycation end products; and increased the levels of tight junction proteins (ZO‐1, occludin, and claudin‐5), low‐density lipoprotein receptor‐related protein 1, and P‐glycoprotein in fibrillar Aβ_1–42‐treated bEnd.3 cells. Moreover, catalpol also enhanced soluble Aβ efflux across the fibrillar Aβ_1–42‐treated bEnd.3 cells BBB monolayer model. Altogether, our results suggest that catalpol alleviate fibrillar Aβ_1–42‐induced BBB disruption, enhance soluble Aβ clearance, and offer a feasible therapeutic application in AD treatment.     

Schisandrin C Ameliorates Learning and Memory Deficits by Aβ1–42‐induced Oxidative Stress and Neurotoxicity in Mice

Schisandrin C (SCH‐C) is a main and typical antioxidative lignan isolated from the fruits of Schisandra chinensis (Trucz.) Baill (a widely used traditional Chinese medicine). The present study aimed to characterize the effect of SCH‐C on memory impairment and further research on pathological changes in Aβ_1–42‐induced Alzheimer's disease mice. Mice were administration with SCH‐C daily for 5 days in the lateral cerebral ventricles using sterotaxically implanted cannula. Cognitive functions were assessed by Y‐maze test, active avoidance test and Morris water maze test in all groups, and the level of Aβ_1–42 and neuronal injury induced by Aβ_1–42 were reversed remarkably following SCH‐C treatment compared with sham group; meanwhile the impairment of short‐term or working memory was dramatically improved. In addition, SCH‐C significantly inhibited total cholinesterase (ChEtotal), and increased superoxide dismutase (SOD) and glutathione peroxidase (GSH‐px) activity glutathione (GSH) levels in the hippocampus and cerebral cortex. It can be speculated that SCH‐C offers protection against Aβ_1–42‐induced dysfunction in learning and memory by inhibiting ChEtotal and its antioxidant action. Copyright © 2015 John Wiley & Sons, Ltd.     

Inhibitory Effects of Key Compounds Isolated from Corni fructus on BACE1 Activity

Progressive cerebral deposition of Aβ in the brain is a seminal event in the pathogenesis of Alzheimer's disease (AD). Aβ is generated from the amyloid precursor protein (APP) by proteolytic processing of β‐secretase (BACE1) and γ‐secretase. Consequently, BACE1, a key enzyme in the production of Aβ, is a prime target for therapeutic intervention in AD. In the course of screening for natural BACE1 inhibitors from Corni fructus, the ethyl acetate (EtOAc) fraction showed significant inhibitory activity against BACE1. By activity guided purification, three compounds of BACE1 inhibitors p‐coumaric acid, gallic acid and ursolic acid were isolated from Corni fructus EtOAc fraction. All isolated compounds suppressed BACE1 in a dose dependent manner. p‐Coumaric acid, in particular, exhibited significant inhibitory activity against BACE1 with 9.0 × 10^‐5 m and a K_i value of 1.9 × 10^‐6 m . Also this compound was non‐competitive with a substrate in the Dixon plot, suggesting that it might bind either to the β‐secretase subsite or to another regulatory site. All compounds showed no significant attenuation of TACE (α‐secretase) and other serine proteases such as chymotrypsin and trypsin, demonstrating that they were relatively selective and specific inhibitors of BACE1. These novel findings suggest that Corni fructus contains biologically active components that may be used to attenuate the progression and/or prevention of Alzheimer's disease. Copyright © 2012 John Wiley & Sons, Ltd.     

A Comparative Study on the Inhibitory Effects of Different Parts and Chemical Constituents of Pomegranate on α‐Amylase and α‐Glucosidase

Pomegranate has been documented for the management of diabetes in Unani and Chinese medicine. This study compared the effects of the extracts of different pomegranate parts, including juice, peels, seeds and flowers, on carbohydrate digestive enzymes (α‐amylase and α‐glucosidase) in vitro. The methanolic flower extract inhibited α‐amylase and α‐glucosidase, while the methanolic peel extract inhibited α‐glucosidase selectively. The most active flower extract was subjected to water‐ethyl acetate partition. The ethyl acetate fraction was more potent than the water fraction in inhibiting both enzymes. Gallic acid and ellagic acid also showed selective inhibition against α‐glucosidase, and their presence in the ethyl acetate fraction was confirmed by HPLC‐DAD and HPLC‐HESI‐MS. Our findings suggest that the inhibition of carbohydrate digestive enzymes and their phenolic content may contribute to the anti‐hyperglycaemic effects of pomegranate flower and peel, and support their claims in diabetes. Copyright © 2012 John Wiley & Sons, Ltd.     

Decursin attenuates the amyloid‐β‐induced inflammatory response in PC12 cells via MAPK and nuclear factor‐κB pathway

Decursin, the major bioactive component of Angelica gigas Nakai, exhibited neuroprotective properties. Our previous studies showed that decursin conferred neuroprotective effects in PC12 cells induced by Amyloid‐β (Aβ)_25–35 via antiapoptosis and antioxidant. In this study, the antiinflammatory effects of decursin against PC12 cells injury stimulated by Aβ_25–35 were assessed. Our results demonstrated that decursin suppressed the expression of cyclooxygenase‐2 protein and prostaglandin E2 content which was stimulated by Aβ_25–35 in PC12 cells. Meanwhile, the nuclear translocation of nuclear factor‐κB in Aβ_25–35‐treated PC12 cells was also inhibited by decursin. In addition, decursin suppressed phosphorylation of the two upstream pathway kinases, p38 and c‐Jun N‐terminal kinase. Overall, our findings indicate that decursin exerts protective effects against neuroinflammation stimulated by Aβ_25–35 in PC12 cells by abolishing cyclooxygenase‐2 protein expression through inactivation of nuclear factor‐κB via the upstream kinases including p38 and c‐Jun N‐terminal kinase. This work provides a new insight into the pharmacological mode of decursin and should facilitate its therapeutic application in treatment of inflammatory disorders.     

Baicalein enhances the antitumor efficacy of docetaxel on nonsmall cell lung cancer in a β‐catenin‐dependent manner

The side effects of docetaxel have limited its antitumor performances in the treatment of nonsmall cell lung cancer (NSCLC). To address the problem, baicalein, a bioactive flavone that exhibits antitumor activity, was combined with docetaxel so as to achieve better efficacy and lower toxicity. The combination treatment enhanced the stabilization of microtubules and halted the cell‐cycle progression, thus synergistically inhibiting the proliferation and inducing the apoptosis of A549 cells and Lewis lung carcinoma cells. The decreased expression of Cyclin‐dependent kinase 6 and Cyclin B1 confirmed its regulation in cell cycle, with β‐catenin being an important upstream effector, as evidenced by the decreased expression in the cytoplasm and nucleus as well as the attenuated aggregation in the nucleus. Furthermore, baicalein plus docetaxel evinced better antitumor efficacy by the suppressed tumor growth, increased apoptosis, and decreased tumor angiogenesis in vivo, with no increased toxicity discovered in both tumor‐bearing and non‐tumor‐bearing mice, and an improvement in therapeutic index. This study has demonstrated that baicalein plus docetaxel is an appropriate combination simultaneously with augmented antitumor efficacy and acceptable safety, which might be a promising strategy for patients with advanced NSCLC.     

Luteoloside attenuates anoxia/reoxygenation‐induced cardiomyocytes injury via mitochondrial pathway mediated by 14‐3‐3η protein

Ischemia/reperfusion (I/R) injury is the major cause of acute cardiovascular disease worldwide. 14‐3‐3η protein has been demonstrated to protect myocardium against I/R injury. Luteoloside (Lut), a flavonoid found in many Chinese herbs, exerts myocardial protection effects. However, the mechanism remains unclear. We hypothesize that the cardioprotective role of Lut is exerted by regulating the 14‐3‐3η signal pathway. To investigate our hypothesis, an in vitro I/R model was generated in H9C2 cardiomyocytes by anoxia/reoxygenation (A/R) treatment. The effects of Lut on cardiomyocytes with A/R injury were assessed by determining the cell viability, lactate dehydrogenase levels, intracellular reactive oxygen species levels, mitochondrial permeability transition pores (mPTP) openness, caspase‐3 activity, and apoptosis rate. The effects on protein expression were tested using western blot analysis. Lut attenuated A/R‐induced injury to cardiomyocytes by increasing the expression of 14‐3‐3η protein and cell viability; decreasing levels of lactate dehydrogenase, reactive oxygen species, mPTP openness, caspase‐3 activity, and low apoptosis rate were observed. However, the cardioprotective effects of Lut were blocked by AD14‐3‐3ηRNAi, an adenovirus knocking down the intracellular 14‐3‐3η expression. In conclusion, to our knowledge, this is the first study to demonstrate that Lut protected cardiomyocytes from A/R‐induced injury via the regulation of 14‐3‐3η signaling pathway.     

Inhibitory Effect of Ethanol Extract of Magnolia officinalis on Memory Impairment and Amyloidogenesis in a Transgenic Mouse Model of Alzheimer's Disease via Regulating β‐Secretase Activity

Alzheimer's disease (AD) is the most common form of dementia and is characterized by deposition of amyloid beta (Aβ) in the brain. The components of the herb Magnolia officinalis are known to have antiinflammatory, antioxidative and neuroprotective activities. In this study we investigated the effects of ethanol extract of M. officinalis on memory dysfunction and amyloidogenesis in a transgenic mouse model of AD. Oral pretreatment of ethanol extract of M. officinalis (10 mg/kg in 0.05% ethanol) into drinking water for 3 months inhibited memory impairment and Aβ deposition in the brain of Tg2576 mice. Ethanol extract of M. officinalis also decreased activity of β‐secretase, cleaving Aβ from amyloid precursor protein (APP), and expression of β‐site APP cleaving enzyme 1 (BACE1), APP and its product, C99. Our results showed that ethanol extract of M. officinalis effectively prevented memory impairment via down‐regulating β‐secretase activity. Copyright © 2012 John Wiley & Sons, Ltd.     

Palbinone,a novel terpenoid from Paeonia albiflora: A potent inhibitory activity on human monocyte interleukin-1β

Palbinone, a novel terpenoid from the roots of Paeonia albiflora, has a very strong inhibitory activity on the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) linked 3α-hydroxysteroid dehydrogenase (3α-HSD) of rat liver cytosol and showed a significant inhibitory activity on human monocyte interleukin-1β, a polypeptide which is though to play an important role in inflammation. In contrast the enzymes cyclooxygenase (CO), thromboxane A synthase (TX) and 5-lipoxygenase (LO) were not significantly inhibited by palbinone when it was compared with tenokisicum, indomethacin, imidazole and 2, 3, 5-trimethyl-6-(12-hydroxy-5, 10-dodecadiynyl)-1, 4-benzoquinone (AA-861) as positive controls under similar experimental conditions. The activity of palbinone was highly selective since it inhibited strongly only human monocyte interleukin-1β and did not show any significant activity on CO, TX and LO.     

Genistein inhibits Aβ25–35‐induced SH‐SY5Y cell damage by modulating the expression of apoptosis‐related proteins and Ca2+ influx through ionotropic glutamate receptors

In this study, we investigated the protective effects of genistein against SH‐SY5Y cell damage induced by β‐amyloid 25–35 peptide (Aβ_25–35) and the underlying mechanisms. Aβ‐induced neuronal death, apoptosis, glutamate receptor subunit expression, Ca²⁺ ion concentration, amino acid transmitter concentration, and apoptosis‐related factor expression were evaluated to determine the effects of genistein on Aβ‐induced neuronal death and apoptosis. The results showed that genistein increased the survival of SH‐SY5Y cells and decreased the level of apoptosis induced by Aβ_25–35. In addition, genistein reversed the Aβ_25–35‐induced changes in amino acid transmitters, α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionate (AMPA) receptors, and N‐methyl‐d ‐aspartate (NMDA) receptor subunits in SH‐SY5Y cells. Aβ_25–35‐induced changes in Ca²⁺ and B‐cell lymphoma‐2 (Bcl‐2) and Bcl‐2‐associated X (Bax) protein and gene levels in cells were also reversed by genistein. Our data suggest that genistein protects against Aβ_25–35‐induced damage in SH‐SY5Y cells, possibly by regulating the expression of apoptosis‐related proteins and Ca²⁺ influx through ionotropic glutamate receptors.     

Effects of Lonicera japonica Thunb. on Type 2 Diabetes via PPAR‐γ Activation in Rats

Lonicera japonica Thunb. (Caprifoliaceae) is a traditional herbal medicine and has been used to treat diabetic symptoms. Notwithstanding its use, the scientific basis on anti‐diabetic properties of L. japonica is not yet established. This study is designed to investigate anti‐diabetic effects of L. japonica in type 2 diabetic rats. L. japonica was orally administered at the dose of 100 mg/kg in high‐fat diet‐fed and low‐dose streptozotocin‐induced rats. After the treatment of 4 weeks, L. japonica reduced high blood glucose level and homeostatic model assessment of insulin resistance in diabetic rats. In addition, body weight and food intake were restored by the L. japonica treatment. In the histopathologic examination, the amelioration of damaged β‐islet in pancreas was observed in L. japonica‐treated diabetic rats. The administration of L. japonica elevated peroxisome proliferator‐activated receptor gamma and insulin receptor subunit‐1 protein expressions. The results demonstrated that L. japonica had anti‐diabetic effects in type 2 diabetic rats via the peroxisome proliferator‐activated receptor gamma regulatory action of L. japonica as a potential mechanism. Copyright © 2015 John Wiley & Sons, Ltd.     

Protective and Therapeutic Effect of the Indonesian Medicinal Herb Curcuma xanthorrhiza on β-D-Galactosamine-induced Liver Damage

The present study was carried out to investigate the hepatoprotective effects of a dose of C. xanthorrhiza on acute hepatotoxicity induced in rats by a single dose of β-D -galactosamine (288 mg/kg, i.p.), and its mechanism of action. C. xanthorrhiza (100 mg/kg) was administered p.o. to experimental animals according to the protocol followed by the i.p. administration of a single dose of hepatotoxin. Hepatoprotective activity was monitored by estimating serum glutamate oxaloacetate transaminase (SGOT) and serum glutamate pyruvate transaminase (SGPT) levels and histopathological changes in the livers of C. xanthorrhiza -treated and untreated groups of animals. The results clearly indicated that the extract of C. xanthorrhiza significantly reduced the acute elevation of serum transaminases induced by hepatotoxin, and alleviated the degree of liver damage at 24 h after the intraperitoneal administration of the hepatotoxins.