Search

We previously reported that Yulangsan polysaccharide (YLSP), which was isolated from the root of Millettia pulchra Kurz, attenuates withdrawal symptoms of morphine dependence by regulating the nitric oxide pathway and modulating monoaminergic neurotransmitters. In this study, we investigated the effects and mechanism of YLSP on the reinstatement of morphine-induced conditioned place preference (CPP) in rats. A CPP procedure was employed to assess the behavior of rats, and indicators of serum and four brain regions (nucleus accumbens, ventral tegmental area, hippocampus and prefrontal cortex) were determined to explore its underlying mechanism. YLSP inhibited priming morphine-induced reinstatement of CPP in a dose-dependent manner. YLSP markedly reduced nitric oxide and nitric oxide synthase levels in the brain. Moreover, YLSP significantly decreased the dopamine and norepinephrine levels in the serum and brain. Furthermore, YLSP significantly decreased cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) concentrations, inhibited the expression of dopamine D1 receptors and cAMP response element binding protein mRNA, and improved the expression of dopamine D2 receptor mRNA in the four brain regions. Our findings indicated that YLSP could inhibit the reinstatement of morphine-induced CPP possibly by modulating the NO-cGMP and D1R-cAMP signaling pathways. [ABSTRACT FROM AUTHOR]

Sarcoma is one of the most prevalent pediatric tumors and the therapeutic role of chemotherapy has yet to be elucidated. It has been reported that extracts of Longyanshen (Yulangsan) may enhance the sensitivity of drug-resistant cancer cell lines, and improve the immune dysfunction induced by cyclophosphamide (CTX) in mice. The present in vivo study investigated the antitumor effects of Yulangsan polysaccharides (YLSPS) and their interaction with CTX in murine sarcoma 180 (S180)-bearing mice. Immunohistochemistry was used to detect the expression of apoptosis-related proteins. The ultrastructure of sarcoma cells was examined by transmission electron microscopy and the tumor growth rate was determined by measuring the tumor weight. A dose-dependent inhibition of sarcoma growth was observed in S180-bearing mice following administration of YLSPS. In combination with CTX, an additive antitumor effect was obtained, which was accompanied by amelioration of immune function. YLSPS also potentiated the tumor suppression effect of CTX while avoiding cytotoxicity against immune cells. YLSPS inhibited sarcoma growth in S180-bearing mice through the induction of apoptosis in S180 sarcoma cells. YLSPS also attenuated CTX-induced cytotoxicity to the immune system while potentiating the tumor suppression effect. These results provide additional information regarding combination therapy with YLSPS and chemotherapy for the treatment of sarcoma. [ABSTRACT FROM AUTHOR]

Active polysaccharides have unique advantages in inhibiting cancer cell proliferation, invasion and metastasis and inducing apoptosis. Yulangsan polysaccharide (YLSPS) is derived from the root of Millettia pulchra var. laxior (Dunn) Z. Wei. Previous studies revealed that YLSPS exhibits bioactivities such as antibacterial, antidepressive, antitumor, hepatoprotective and immunomodulating activities. However, the anticancer effects of YLSPS on lung cancer have not yet been studied, and its mechanism of action remains unclear. The present study investigated the anti-migration/invasion effects of YLSPS and possible mechanisms in lung cancer cells (A549 and Lewis) in vitro and in vivo . The data suggested that YLSPS reversed epithelial-mesenchymal transition (EMT) and inhibited the invasion and migration of lung cancer cells by inhibiting the TGF-β1-induced ERK signaling pathway. Furthermore, YLSPS reduced the levels of proteins associated with EMT, including vimentin, but increased those of E-cadherin, as determined by Western blotting. In vivo , YLSPS significantly inhibited the growth of xenograft tumors, and decreased the levels of TGF-β1 and protein markers associated with EMT. Importantly, YLSPS had fewer toxic side effects than cisplatin. Overall, YLSPS significantly delayed non-small cell lung cancer (NSCLC) progression by modulating EMT and TGF-β1/ERK signaling pathway. The present findings suggest that YLSPS may be a potential adjuvant therapy and drug for improving the tumor microenvironment of lung cancer., Competing Interests: None., (AJCR Copyright © 2023.)

Ethnopharmacological relevance Millettia pulchra Kurz var-laxior (Dunn) Z. Wei, a wild-growing plant of the family Fabaceae is known to possess multifarious medicinal properties. Yulangsan polysaccharide (YLSPS) is a chief ingredient of its root, which has been used in Chinese traditional medicine with a long history for remedy of acute or chronic hepatitis and jaundice. Aim of the study To investigate the ability of the YLSPS to protect against diclofenac-induced hepatotoxicity in mice. Materials and methods Mice were orally treated with YLSPS daily 1 h after the injection of diclofenac for 2 weeks. Dimethyl diphenyl bicarboxylate was used as a reference drug. Results YLSPS effectively reduced the elevated levels of serum alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase and enhanced the reduction of superoxide dismutase, catalase, and glutathione peroxidase activities in the liver. Moreover, the content of malondialdehyde was reduced by treatment with YLSPS, and histological findings also confirmed the anti-hepatotoxic activity. In addition, YLSPS significantly inhibited proinflammatory mediators, such as tumor necrosis factor-alpha and interleukin 1 beta. YLSPS also enhanced mitochondrial antioxidants and inhibited cell death by preventing the down-regulation of Bcl-2 and the up-regulation and release of Bax along with caspase 9 and 3 activity; thus, these findings confirm the involvement of mitochondria in diclofenac-induced apoptosis. Conclusion The results indicate that protective effects of YLSPS against diclofenac-induced acute hepatic injury may rely on its effect on reducing oxidative stress, suppressing inflammatory responses, and improving drug-metabolizing enzyme activity in the liver. [ABSTRACT FROM AUTHOR]

Although numerous studies have proven the medicinal values of Yulangsan polysaccharide (YLSP), the toxicity of this active ingredient is unknown. In the acute toxicity study, a single oral administration of 24 g/kg YLSP caused neither toxicological symptoms nor mortality, and the LD 50 was estimated >24 g/kg. In the chronic toxicity study, we administered doses of 0, 0.6, 1.2 and 2.4 g/kg YLSP in rats by oral gavage for 26 weeks followed by a 3-week recovery period. There was no mortality or remarkable clinical signs observed during this 26-week study. Additionally, there were no toxic differences in the following parameters: body weight, food consumption, hematology, clinical biochemistry, organ weight, and macroscopic findings. There were no adverse effects on histopathology observed in males or female rats treated with YLSP. Based on the results, the no-observed-adverse-effect-level of YLSP in rats is greater than 2.4 g/kg when administered orally for 26 consecutive weeks. [ABSTRACT FROM AUTHOR]

Ethnopharmacological relevance Yulangsan polysaccharide (YLSPS) is often used in popular folk medicine in the Guangxi Zhuang Autonomous Region of China as a chief ingredient of Millettia pulchra , which is used as a hepatic protection, anti-aging and memory improving agent. Aim of the study This study was designed to investigate the protective effects of polysaccharides from Millettia pulchra Kurz var.laxior (Dunn) (Yulangsan polysaecharide, YLSPS) against nimesulide-induced hepatotoxicities in mice. Materials and methods Liver injury was induced in mice by administering nimesulide. Simultaneously, YLSPS was administered 2 h prior to the administration of nimesulide. Dimethyl diphenyl bicarboxylate (DDB) was used as a reference drug. Results Compared with the nimesulide group, YLSPS significantly decreased the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and the content of bilirubin in the serum. The anti-oxidative effect of YLSPS was observed from the increase of the superoxide dismutase (SOD) and catalase and glutathione peroxidase (GSH-Px) activities in the liver, both of which were decreased by nimesulide. Moreover, the content of malondialdehyde (MDA) was reduced, and histological findings also confirmed the anti-hepatotoxic activity. In addition, YLSPS significantly inhibited proinflammatory mediators, such as tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6). Additionally, YLSPS also enhanced the mitochondrial antioxidant and inhibited dead cells by preventing the down-regulation of Bcl-2, up-regulation and release of Bax along with caspase 9 and 3 activity, confirming the involvement of mitochondria in the nimesulide-induced apoptosis. Conclusion The protective effect of YLSPS against nimesulide-induced hepatic injury may rely on its ability to reduce oxidative stress and prevent nimesulide-induced hepatotoxicity by inhibiting critical control points of apoptosis. [ABSTRACT FROM AUTHOR]

Highlights: [•] YLSP attenuated morphine withdrawal symptoms. [•] YLSP decreased brain NO levels and NOS activity in morphine dependent rats. [•] YLSP modulated the level of DA as well as NE in NAc, VTA, HIP, and PFC. [ABSTRACT FROM AUTHOR]

The article discusses a study on a mouse model of depression induced by unpredictable chronic mild stress. The study used Yulangsan polysaccharide (YLSPS) to treat the model mice. It performed enzyme-linked immunosorbent assay, radioimmunity and immunohistochemical staining following the treatment. It showed the inhibition of depression by YLSPS by upregulating monoamine neurotransmitters and prefrontal cortex adenylate cyclase activity.

Sarcoma is one of the most prevalent pediatric tumors and the therapeutic role of chemotherapy has yet to be elucidated. It has been reported that extracts of Longyanshen (Yulangsan) may enhance the sensitivity of drug-resistant cancer cell lines, and improve the immune dysfunction induced by cyclophosphamide (CTX) in mice. The present in vivo study investigated the antitumor effects of Yulangsan polysaccharides (YLSPS) and their interaction with CTX in murine sarcoma 180 (S180)-bearing mice. Immunohistochemistry was used to detect the expression of apoptosis-related proteins. The ultrastructure of sarcoma cells was examined by transmission electron microscopy and the tumor growth rate was determined by measuring the tumor weight. A dose-dependent inhibition of sarcoma growth was observed in S180-bearing mice following administration of YLSPS. In combination with CTX, an additive antitumor effect was obtained, which was accompanied by amelioration of immune function. YLSPS also potentiated the tumor suppression effect of CTX while avoiding cytotoxicity against immune cells. YLSPS inhibited sarcoma growth in S180-bearing mice through the induction of apoptosis in S180 sarcoma cells. YLSPS also attenuated CTX-induced cytotoxicity to the immune system while potentiating the tumor suppression effect. These results provide additional information regarding combination therapy with YLSPS and chemotherapy for the treatment of sarcoma.

The present study established a mouse model of depression induced by unpredictable chronic mild stress. The model mice were treated with Yulangsan polysaccharide (YLSPS; 150, 300 and 600 mg/kg) for 21 days, and compared with fluoxetine-treated and normal control groups. Enzyme-linked immunosorbent assay, radioimmunity and immunohistochemical staining showed that following treatment with YLSPS (300 and 600 mg/kg), monoamine neurotransmitter levels, prefrontal cortex adenylate cyclase activity and hippocampal brain-derived neurotrophic factor expression were significantly elevated, and depression-like behaviors were improved. Open-field and novelty-suppressed feeding tests showed that mouse activity levels were increased and feeding latency was shortened following treatment. Our results indicate that YLSPS inhibits depression by upregulating monoamine neurotransmitters, prefrontal cortex adenylate cyclase activity and hippocampal brain-derived neurotrophic factor expression.