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The aim of the present study was to investigate the effects of Lycium barbarum polysaccharides (LBP) on cisplatin-induced hair cell damage in the organ of Corti explant. The neonatal (P2-3) rat organ of Corti explant was exposed to cisplatin (20 μM; 48 h) with or without LBP pretreatment (150 and 600 μg/mL; 24 h). Hair cell loss was indicated by FITC-labeled phalloidin staining. The level of reactive oxygen species (ROS) and alteration of mitochondrial membrane potential (ΔΨ(m)) in hair cells were analyzed using fluorescent probes 2',7'-dichlorofluorescein diacetate and JC-1, respectively. The results showed that LBP significantly attenuated hair cell loss (p < 0.01). Hair cells pretreated with LBP showed significant reduction in ROS production and the decline of ΔΨ(m) compared with cisplatin alone group (p < 0.01), indicating the protective effect of LBP on cisplatin-induced hair cell loss. Taken together, these results indicate that LBP was effective in attenuating cisplatin-induced hair cell loss by reducing the production of ROS and maintaining mitochondrial ΔΨ(m).

Lycium barbarum polysaccharide (LBP) is the main active component of Fructus Lycii, exhibiting various biological activities. This study aims to explore the protective effects of LBP on human corneal epithelial cells (HCEC) and a rat corneal injury model. Potential target points for LBP improving corneal injury repair were screened from public databases, and functional and pathway enrichment analyses of core targets were conducted using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). Rat corneal alkali burns and HCEC oxidative stress injury models were established, and the results were validated through slit lamp examination, HE staining, TUNEL assay, immunofluorescence, CCK-8 assay, flow cytometry, scratch assay, and qRT-PCR methods. In the context of database retrieval, identification of 10 LBP monosaccharide components and 50 corneal injury repair-related targets was achieved. KEGG pathway analysis suggested that LBP might regulate the IL-17 and TNF signaling pathways through targets such as JUN, CASP3, and MMP9, thereby improving corneal damage. In vivo and in vitro experimental results indicated that LBP could reduce the increase of inflammation index scores (p < 0.05), inflammatory cell density (p < 0.01), TUNEL-positive cells (p < 0.01), corneal opacity scores (p < 0.01), and expression of corneal stromal fibrosis-related proteins α-SMA, FN, and COL (p < 0.01) caused by chemical damage to rat corneas. LBP inhibited oxidative stress-induced decreases in cell viability (p < 0.001) and migration healing ability (p < 0.01) in HCECs, reducing apoptosis rates (p < 0.001), ROS levels (p < 0.001), and the expression of inflammatory factors TNF-α and IL-6 (p < 0.01). qRT-PCR results demonstrated that LBP intervention decreased the mRNA levels of JUN, CASP3, and MMP9 in H2O2-induced alkaline-burned corneas and HCECs (p < 0.01).The integrated results from network pharmacology and validation experiments suggest that the inhibitory effects of LBP on apoptosis, inflammation, and fibrosis after corneal injury may be achieved through the suppression of the TNF and IL-17 signaling pathways mediated by JUN, CASP3, and MMP9. [ABSTRACT FROM AUTHOR]

The effects of Lycium barbarum polysaccharides (LBP) and plasmon-activated water (PAW) against IFN-γ/TNF-α induced inflammation in human colon Caco-2 cells were investigated. Cells were divided into the control, induction, LBP treatment (100–500 μg/mL), and combination groups with PAW. Inflammation was induced 24 h with 10 ng/mL IFN-γ when cell confluency reached >90%, and various doses of LBP with or without PAW were treated for 3 h, and subsequently 50 ng/mL TNF-α was added for another 24 h to provoke inflammation. Combination of LBP with PAW significantly decreased the secretion of IL-6 and IL-8. Cyclooxygenase-2 and inducible NO synthase expression was attenuated in all LBP-treated groups with or without PAW. NLRP3 inflammasome and related protein PYCARD expression were inhibited by LBP at the highest dose (500 μg/mL). All doses of LBP alone significantly decreased p-ERK expression, but combination with PAW increased p-ERK expression compared to those without PAW. Additionally, 250 and 500 μg/mL of LBP with or without PAW inhibited procaspase-3/caspase-3 expression. Therefore, LBP possesses anti-inflammation and anti-apoptosis by inhibiting the secretion of inflammatory cytokines and the expression of NLRP3 inflammasome-related protein. The combination with PAW exerts additive or synergistic effect on anti-inflammation. [ABSTRACT FROM AUTHOR]

BACKGROUND: A large number of studies have shown that neurodegenerative diseases are closely related to oxidative stress injury and the imbalance of mitochondrial dynamics. Lycium barbarum polysaccharides have a neuroprotective effect. However, it is not clear whether lycium barbarum polysaccharides can ameliorate apoptosis induced by oxidative stress injury by regulating abnormal mitochondrial dynamics. OBJECTIVE: To study the effect of lycium barbarum polysaccharides on apoptosis induced by H2O2 in SH-SY5Y human neuroblastoma cells. METHODS: SH-SY5Y cells were cultured in three groups. The control group was cultured for 24 hours. The hydrogen peroxide group was treated with H2O2 for 24 hours, and the lycium barbarum polysaccharide group was treated with lycium barbarum polysaccharide for 2 hours and then treated with H2O2 for 24 hours. After treatment, the levels of malondialdehyde, glutathione, and superoxide dismutase in the precipitation of the cells were detected by kit. Mitochondrial membrane potential was detected by JC-1 kit. Cell viability was detected by MTT assay. Apoptosis was detected by TUNEL. The expression levels of mitochondrial dynamicsrelated proteins (phosphorylated promoter protein 1, mitochondrial fission protein 1, mitochondrial fusion protein 1, mitochondrial fusion protein 2, and optic atrophy protein 1) and apoptotic proteins (Bax, Bcl-2, and Caspase-3) were detected by immunofluorescence staining and western blot assay. RESULTS AND CONCLUSION: (1) Compared with the control group, the levels of malondialdehyde were increased (P < 0.05), and the levels of superoxide dismutase and glutathione were decreased (P < 0.05) in the H2O2 group. Compared with the H2O2 group, the malondialdehyde level was decreased (P < 0.05), and the superoxide dismutase and glutathione levels were increased (P < 0.05) in the lycium barbarum polysaccharide group. (2) The mitochondrial membrane potential in the H2O2 group was lower than that in the control group (P < 0.05), and that of lycium barbarum polysaccharide group was higher than that of the H2O2 group (P < 0.05). (3) Compared with the control group, the apoptosis rate and the expression of Bax and Caspase-3 protein were increased (P < 0.05), while the cell viability and the expression of Bcl-2 protein were decreased (P < 0.05) in the H2O2 group. Compared with the H2O2 group, the apoptosis rate and the expression of Bax and Caspase-3 protein were decreased (P < 0.05), while the cell viability and the expression of Bcl-2 protein were increased (P < 0.05) in the lycium barbarum polysaccharide group. (4) Compared with the control group, the protein expression levels of phosphorylated promoter protein 1 and mitochondrial fission protein 1 were increased (P < 0.05), and the protein expression levels of mitochondrial fusion protein 1, mitochondrial fusion protein 2, and optic atrophy protein 1 were decreased (P < 0.05) in the H2O2 group. Compared with the H2O2 group, the protein expression levels of phosphorylated promoter protein 1 and mitochondrial fission protein 1 were decreased (P < 0.05), and the protein expression levels of mitochondrial fusion protein 1, mitochondrial fusion protein 2, and optic atrophy protein 1 were increased (P < 0.05) in the lycium barbarum polysaccharide group. (5) These results indicate that lycium barbarum polysaccharide can improve SH-SY5Y cell apoptosis caused by oxidative stress damage by regulating mitochondrial dynamics. [ABSTRACT FROM AUTHOR]

Pancreatic β-cells death mediated by apoptosis plays a key role in the development of diabetes. Pro-inflammatory cytokines activate the apoptotic program in pancreatic β-cells. Therefore, inhibiting inflammatory cytokines induced apoptosis could preserve pancreatic β-cells. The fruit of Lycium is widely used as an antioxidant food and its pharmacological action is partially mediated by Lycium barbarum polysaccharides (LBP). However, whether LBP can inhibit inflammatory cytokines-induced β-cells apoptosis has not been reported. In this study, we showed that LBP could alleviate the apoptosis of pancreatic β-cells through the inhibition of interferon-γ (IFN-γ) pathway. In healthy mice, LBP administration could improve glucose tolerance. In streptozotocin-induced β-cells injury mice, preventive and continuous administration of LBP could alleviate hyperglycemia and protect pancreatic insulin content. Our study identified a novel function of LBP in prevention and protection of pancreatic β-cells apoptosis, which was partially through the inhibition of IFN-γ pathway.

Lycium barbarum polysaccharide (LBP) is the main active component of Fructus Lycii, exhibiting various biological activities. This study aims to explore the protective effects of LBP on human corneal epithelial cells (HCEC) and a rat corneal injury model. Potential target points for LBP improving corneal injury repair were screened from public databases, and functional and pathway enrichment analyses of core targets were conducted using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). Rat corneal alkali burns and HCEC oxidative stress injury models were established, and the results were validated through slit lamp examination, HE staining, TUNEL assay, immunofluorescence, CCK-8 assay, flow cytometry, scratch assay, and qRT-PCR methods. In the context of database retrieval, identification of 10 LBP monosaccharide components and 50 corneal injury repair-related targets was achieved. KEGG pathway analysis suggested that LBP might regulate the IL-17 and TNF signaling pathways through targets such as JUN, CASP3, and MMP9, thereby improving corneal damage. In vivo and in vitro experimental results indicated that LBP could reduce the increase of inflammation index scores (p < 0.05), inflammatory cell density (p < 0.01), TUNEL-positive cells (p < 0.01), corneal opacity scores (p < 0.01), and expression of corneal stromal fibrosis-related proteins α-SMA, FN, and COL (p < 0.01) caused by chemical damage to rat corneas. LBP inhibited oxidative stress-induced decreases in cell viability (p < 0.001) and migration healing ability (p < 0.01) in HCECs, reducing apoptosis rates (p < 0.001), ROS levels (p < 0.001), and the expression of inflammatory factors TNF-α and IL-6 (p < 0.01). qRT-PCR results demonstrated that LBP intervention decreased the mRNA levels of JUN, CASP3, and MMP9 in H2O2-induced alkaline-burned corneas and HCECs (p < 0.01).The integrated results from network pharmacology and validation experiments suggest that the inhibitory effects of LBP on apoptosis, inflammation, and fibrosis after corneal injury may be achieved through the suppression of the TNF and IL-17 signaling pathways mediated by JUN, CASP3, and MMP9.

The effects of Lycium barbarum polysaccharides (LBP) and plasmon-activated water (PAW) against IFN-γ/TNF-α induced inflammation in human colon Caco-2 cells were investigated. Cells were divided into the control, induction, LBP treatment (100–500 μg/mL), and combination groups with PAW. Inflammation was induced 24 h with 10 ng/mL IFN-γ when cell confluency reached >90%, and various doses of LBP with or without PAW were treated for 3 h, and subsequently 50 ng/mL TNF-α was added for another 24 h to provoke inflammation. Combination of LBP with PAW significantly decreased the secretion of IL-6 and IL-8. Cyclooxygenase-2 and inducible NO synthase expression was attenuated in all LBP-treated groups with or without PAW. NLRP3 inflammasome and related protein PYCARD expression were inhibited by LBP at the highest dose (500 μg/mL). All doses of LBP alone significantly decreased p-ERK expression, but combination with PAW increased p-ERK expression compared to those without PAW. Additionally, 250 and 500 μg/mL of LBP with or without PAW inhibited procaspase-3/caspase-3 expression. Therefore, LBP possesses anti-inflammation and anti-apoptosis by inhibiting the secretion of inflammatory cytokines and the expression of NLRP3 inflammasome-related protein. The combination with PAW exerts additive or synergistic effect on anti-inflammation.

Aspirin causes gastrotoxicity and damaged epithelial defense via cyclooxygenase inhibition. C-phycocyanin (CPC) and Lycium barbarum polysaccharides (LBP), an active ingredient of Spirulina platensis and wolfberry, respectively, exerted antioxidation, anti-inflammation, and/or immunoregulation. The actions of CPC and/or LBP on gastric damage induced by aspirin were explored in rat gastric mucosal RGM-1 cells. Gastric injury was performed by 21 mM aspirin for 3 h after the pretreatment of CPC and/or LBP (100–500 μg/mL) for 24 h in RGM-1 cells. Proinflammatory, anti-inflammatory, and apoptotic markers were examined by ELISA or gel electrophoresis and Western blotting. Cell viability and interleukin 10 (IL-10) were reduced by aspirin. Increased proinflammatory markers, caspase 3 activity, and Bax protein were observed in RGM-1 cells with aspirin treatment. Aspirin elevated nuclear factor-κB (NF-κB), extracellular signal-regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK) activation, while CPC and/or LBP increased IL-10, and attenuated proinflammatory markers, Bax protein, NF-κB, and the activation of ERK and JNK. Therefore, CPC and/or LBP possess anti-inflammation by restraining the activation of the ERK signaling pathway, and LBP decreases apoptosis by suppressing the JNK signaling pathway activation in gastric RGM-1 cells with aspirin-induced epithelial damage. [ABSTRACT FROM AUTHOR]

Lycium barbarum polysaccharides (LBPs) are beneficial for vision; however, relevant research has mainly focused on entire crude polysaccharides, with the basis and exact structure of the polysaccharide rarely explored. In this study, LICP009-3F-2a, a novel polysaccharide from Lycium barbarum L., was separated and then purified using anion-exchange and size-exclusion chromatography. Structural characteristics were investigated using chemical and spectroscopic methods, which revealed that LICP009-3F-2a has an Mw of 13720 Da and is an acidic heteropolysaccharide composed of rhamnose (39.1%), arabinose (7.4%), galactose (22.5%), glucose (8.3%), galacturonic acid (13.7%), and glucuronic acid (4.0%). Linkage and NMR data revealed that LICP009-3F-2a has the following backbone: →2)-α-L-Rha-(1 → 2,4)-α-L-Rha-(1 → 4)-α-D-GalA p -(1 → 3,6)-β-D-Gal p -(1 → 3,6)-β-D-Gal p -(1 → 6)-β-D-Gal p -(1→, with three main branches, including: α-L-Ara f -(1 → 5)-α-L-Ara f -(1 → 6)-β-D-Glc p -(1 → 2,4)-α-L-Rha-(1→, β-D-Glc p -(1 → 4)-β-D-Glc p -(1 → 3,6)-β-D-Gal p -(1→, and β-D-Gal p -(1 → 3)-β-D-Gal p -(1 → 3,6)-β-D-Gal p -(1 →. Differential scanning colorimetry and thermogravimetric analysis showed that LICP009-3F-2a is thermally stable, while X-ray diffractometry showed that LICP009-3F-2a has a semi-crystalline structure. In addition, LICP009-3F-2a protects ARPE-19 cells from H 2 O 2 -induced oxidative damage by regulating the expression of antioxidant SOD1 and CAT enzymes and down-regulating MMP2 expression. Moreover, LICP009-3F-2a promotes the proliferation of ARPE-19 cells in a concentration-dependent manner, and protects ARPE-19 cells from hyperglycemia by inhibiting apoptosis. [ABSTRACT FROM AUTHOR]

Ischemic stroke and cranial radiotherapy may induce brain inflammatory response, oxidative stress, apoptosis and neuronal loss, and impairment of neurogenesis. Lycium barbarum has anti-oxidation, anti-inflammatory, anti-tumor and anti-aging properties, may produce both neuroprotective and radioprotective effects. In this narrative review paper, we described the neuroprotective effect of Lycium barbarum in different animal models of experimental ischemic stroke and limited studies in irradiated animal models. Relevant molecular mechanisms are also summarized. It has been shown that in experimental ischemic stroke models, Lycium barbarum produces neuroprotective effects by modulating neuroinflammatory factors such as cytokines and chemokines, reactive oxygen species, and neurotransmitter and receptor systems. In irradiation animal models, Lycium barbarum prevents radiation-induced loss of hippocampal interneurons. Given its minimal side-effects, these preclinical studies suggest that Lycium barbarum may be a promising radio-neuro-protective drug that can be used as an adjunct treatment to radiotherapy for brain tumor and in the treatment of ischemic stroke. At molecular levels, Lycium barbarum may regulate PI3K/Akt/GSK-3β, PI3K/Akt/mTOR, PKCε/Nrf2/HO-1, keap1-Nrf2/HO-1, and NR2A and NR2B receptor- related signal transduction pathways to produce neuroprotective effects.

Olive oil and Lycium barbarum polysaccharides were considered to be hepatoprotective for liver fibrosis. This study investigated anti-apoptotic, anti-inflammatory and anti-fibrotic effects of olive oil and/or Lycium barbarum polysaccharides (LBP) on CCl4-induced liver fibrosis in rats. The results showed that CCl4 caused liver fatty change, cell death, inflammation and collagen accumulation. The olive oil-treated groups reduced hepatic transforming growth factor (TGF)-β1 and tissue inhibitors of metalloproteinase (TIMP)-1 levels. The LBP-treated groups inhibited hepatic caspase-9 and caspase-3 activities, decreased hepatic tumor necrosis factor (TNF)-α levels, increased hepatic interleukin (IL)-10 levels and IL-10/TNF-α ratios, and reduced hepatic TGF-β1 and TIMP-1 levels. Olive oil combined with LBP suppressed liver apoptotic markers, inhibited liver inflammatory markers, and attenuated hepatic TGF-β1 levels. Therefore, LBP improves liver apoptotic, inflammatory and fibrotic markers, while olive oil combined with LBP has better effects on anti-apoptosis and anti-inflammation compared with olive oil treatment in rats with CCl4-induced liver fibrosis.

Introduction: Oxidative stress is the main cause of osteoarthritis (OA). Lycium barbarum polysaccharides (LBP) have antioxidant properties. Thus, the potential effect of LBP on H2O2-stimulated chondrocytes was examined.Material and Methods: The cell viability was detected by CCK-8. The reactive oxygen species (ROS) production and apoptosis rates were determined by flow cytometric analysis. The DNA damage was detected by comet assay. Real-time polymerase chain reaction (qPCR) and Western blot assays were performed to examine the expression of histone 2A family member X (γH2AX), checkpoint kinase 1 (Chk1), poly ADP-ribose polymerase (PARP), cysteinyl aspartate specific proteinase (caspase)-3/8/9, and nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and its antioxidant-response element (ARE) dependent factors including heme oxygenase-1 (HO-1) and quinine oxidoreductase-1 (NQO-1).Results: Compared to the H2O2 group, LBP inhibited the ROS production and DNA damage caused by H2O2 (p < 0.05), respectively. LBP inhibited the mRNA and protein expressions of γH2AX and Chk1 (p < 0.05). Meanwhile, LBP significantly decreased apoptosis (p < 0.05). And LBP inhibited the expression levels of PARP and Caspase-3/8/9 (p < 0.05). Moreover, LBP increased the expression of Nrf2, HO-1and NQO-1 (p < 0.05). Furthermore, the depletion of Nrf2 that mediated by RNA interference reversed the apoptosis and DNA damage inhibition effect of LBP (p < 0.05).Conclusions: LBP protected chondrocytes through inhibiting DNA damage and apoptosis caused by H2O2, in which the Nrf2/ARE signaling pathway played a positive role. It provided an inspiration for clinical application - developing LBP as a therapeutic agent and Nrf2 as a promising candidate. [ABSTRACT FROM AUTHOR]

Objective  The aim of this study was to explore the inhibition effect and possible mechanism of Lycium barbarum polysaccharides (LBP) on rat intracerebral hemorrhage (ICH) secondary neuronal apoptosis. Materials and Methods  High-, medium-, and low-dose LBP (50, 100, and 200 mg•kg) and nimodipine (10 mg•kg) groups were given once daily by 15-day gavage before operation, while the sham operation and ICH groups were given the equal volume of saline. An ICH model was established by autologous blood injection and the neurological function in each group was scored at 4, 8, 12, 24, and 48 hours after modeling. Furthermore, terminal deoxynucleotidyl transferase dUTP nick end labeling analysis was performed to detect neuronal apoptosis, while western blot, immunohistochemistry, and real-time-polymerase chain reaction were used to study the influence of LBP on ICH secondary neuronal apoptosis. Results  The neurological function score was significantly decreased after ICH, and the intervention effect of a single drug was not evident. The apoptotic nerve cells increased significantly in the ICH group but decreased considerably in the LBP groups. Furthermore, tumor necrosis factor alpha (TNF-α) expression decreased significantly, while B-cell lymphoma 2 expression increased substantially in the high- and medium-dose LBP groups compared with ICH group, suggesting that LBP could reduce the effect of ICH. However, the impact of LBP did not correlate positively with the dose. Conclusion  The application of LBP may not significantly improve neurological function after ICH, but it can inhibit rat ICH secondary neuronal apoptosis. [ABSTRACT FROM AUTHOR]

Previous studies have demonstrated that ovariectomy may lead to a reduction in antioxidative biomarkers in the myocardium, thus suggesting that estrogens may serve a protective role in the suppression of oxidative stress. Lycium barbarum polysaccharides (LBP) are a well-known antioxidant Chinese traditional medicine, which appear to have a similar function to estrogens with regards to the regulation of cardiac function. In the present study, 30 Sprague-Dawley rats were randomly divided into the following groups: Sham operation group, ovariectomized (OVX) group, estradiol valerate group, high-dose LBP (LBP-H) group and low-dose LBP (LBP-L) group. All of the rats were provided tap water, estradiol valerate or LBP for 12 weeks. In addition, all rats were ovariectomized, with the exception of rats in the sham operation group, which underwent fat removal only. Reactive oxygen species (ROS), malondialdehyde (MDA), glutathione peroxidase (GSH-px), catalase (CAT) and superoxide dismutase activities were subsequently examined. The protein expression levels of cleaved caspase-9, cleaved caspase-3 and phosphorylated-protein kinase B (p-Akt) were also assessed. The results demonstrated that high-dose LBP decreased the enhanced levels of ROS and MDA in OVX rats, whereas GSH-px and CAT activities were increased in the LBP-H group compared with in OVX rats. Furthermore, the expression levels of cleaved caspase-9 and cleaved caspase-3 were significantly upregulated in the OVX group, whereas high-dose LBP exerted protective effects on OVX rats by decreasing the expression of apoptotic proteins. Conversely, p-Akt expression was decreased in the OVX group and was increased in the LBP-H group. These results indicated that LBP is essentially involved in cardiac protection by inhibiting apoptosis in response to oxidative stress. In addition, improvement of antioxidant status by LBP is associated with the Akt signaling pathway in the myocardium of OVX rats. [ABSTRACT FROM AUTHOR]

AIM: To investigate the protective effect and its mechanism of lycium barbarum polysaccharides (LBP) against oxidative stress-induced apoptosis in human retinal pigment epithelial cells. METHODS: ARPE-19 cells, a human retinal pigment epithelial cell lines, were exposed to different concentrations of H2O2 for 24h, then cell viability was measured by Cell Counting Kit-8 (CCK-8) assay to get the properly concentration of H2O2 which can induce half apoptosis of APRE-19. With different concentrations of LBP pretreatment, the ARPE-19 cells were then exposed to appropriate concentration of H2O2, cell apoptosis was detected by flow cytometric analysis. Expression levels of Bcl-2 and Bax were measured by real time quantitative polymerase chain reaction (RT-PCR) technique. RSULTS: LBP significantly reduced the H2O2-induced ARPE-19 cells’ apoptosis. LBP inhibited the H2O2-induced down-regulation of Bcl-2 and up-regulation of Bax. CONCLUSION: LBP could protect ARPE-19 cells from H2O2-induced apoptosis. The Bcl-2 family had relationship with the protective effects of LBP.

Graphical abstract Highlights • Olive oil alleviates liver fibrotic markers in CCl 4 -induced liver fibrosis. • Lycium barbarum polysaccharides improve liver apoptotic, inflammatory and fibrotic markers in CCl 4 -induced liver fibrosis. • Olive oil combined with Lycium barbarum polysaccharides has better effects on anti-apoptosis and anti-inflammation in rats with liver fibrosis induced by CCl 4. Abstract Olive oil and Lycium barbarum polysaccharides were considered to be hepatoprotective for liver fibrosis. This study investigated anti-apoptotic, anti-inflammatory and anti-fibrotic effects of olive oil and/or Lycium barbarum polysaccharides (LBP) on CCl 4 -induced liver fibrosis in rats. The results showed that CCl 4 caused liver fatty change, cell death, inflammation and collagen accumulation. The olive oil-treated groups reduced hepatic transforming growth factor (TGF)-β1 and tissue inhibitors of metalloproteinase (TIMP)-1 levels. The LBP-treated groups inhibited hepatic caspase-9 and caspase-3 activities, decreased hepatic tumor necrosis factor (TNF)-α levels, increased hepatic interleukin (IL)-10 levels and IL-10/TNF-α ratios, and reduced hepatic TGF-β1 and TIMP-1 levels. Olive oil combined with LBP suppressed liver apoptotic markers, inhibited liver inflammatory markers, and attenuated hepatic TGF-β1 levels. Therefore, LBP improves liver apoptotic, inflammatory and fibrotic markers, while olive oil combined with LBP has better effects on anti-apoptosis and anti-inflammation compared with olive oil treatment in rats with CCl 4 -induced liver fibrosis. [ABSTRACT FROM AUTHOR]

[Display omitted] • LBP alleviates apoptosis through IFN-γ pathway in pancreatic β-cells. • Preventive application of LBP can protect streptozotocin induce β-cells death. • LBP improves glucose tolerance in healthy mice. • LBP is a natural product in β-cells protection for whom are susceptible to diabetes. Pancreatic β-cells death mediated by apoptosis plays a key role in the development of diabetes. Pro-inflammatory cytokines activate the apoptotic program in pancreatic β-cells. Therefore, inhibiting inflammatory cytokines induced apoptosis could preserve pancreatic β-cells. The fruit of Lycium is widely used as an antioxidant food and its pharmacological action is partially mediated by Lycium barbarum polysaccharides (LBP). However, whether LBP can inhibit inflammatory cytokines-induced β-cells apoptosis has not been reported. In this study, we showed that LBP could alleviate the apoptosis of pancreatic β-cells through the inhibition of interferon-γ (IFN-γ) pathway. In healthy mice, LBP administration could improve glucose tolerance. In streptozotocin-induced β-cells injury mice, preventive and continuous administration of LBP could alleviate hyperglycemia and protect pancreatic insulin content. Our study identified a novel function of LBP in prevention and protection of pancreatic β-cells apoptosis, which was partially through the inhibition of IFN-γ pathway. [ABSTRACT FROM AUTHOR]

Glutamate excitotoxicity plays an important role in neuronal death after ischemia. However, all clinical trials using glutamate receptor inhibitors have failed. This may be related to the evidence that activation of different subunit of NMDA receptor will induce different effects. Many studies have shown that activation of the intrasynaptic NR2A subunit will stimulate survival signaling pathways, whereas upregulation of extrasynaptic NR2B will trigger apoptotic pathways. A Lycium barbarum polysaccharide (LBP) is a mixed compound extracted from Lycium barbarum fruit. Recent studies have shown that LBP protects neurons against ischemic injury by anti-oxidative effects. Here we first reported that the effect of LBP against ischemic injury can be achieved by regulating NR2B and NR2A signaling pathways. By in vivo study, we found LBP substantially reduced CA1 neurons from death after transient global ischemia and ameliorated memory deficit in ischemic rats. By in vitro study, we further confirmed that LBP increased the viability of primary cultured cortical neurons when exposed to oxygen-glucose deprivation (OGD) for 4 h. Importantly, we found that LBP antagonized increase in expression of major proteins in the NR2B signal pathway including NR2B, nNOS, Bcl-2-associated death promoter (BAD), cytochrome C (cytC) and cleaved caspase-3, and also reduced ROS level, calcium influx and mitochondrial permeability after 4 h OGD. In addition, LBP prevented the downregulation in the expression of NR2A, pAkt and pCREB, which are important cell survival pathway components. Furthermore, LBP attenuated the effects of a NR2B co-agonist and NR2A inhibitor on cell mortality under OGD conditions. Taken together, our results demonstrated that LBP is neuroprotective against ischemic injury by its dual roles in activation of NR2A and inhibition of NR2B signaling pathways, which suggests that LBP may be a superior therapeutic candidate for targeting glutamate excitotoxicity for the treatment of ischemic stroke.

Lycium barbarum has been used in China for more than 2,000 years as a traditional medicinal herb and food supplement. Lycium barbarum contains abundant Lycium barbarum polysaccharides (LBPs), betaine, phenolics, carotenoids (zeaxanthin and ß-carotene), cerebroside, 2-O-ß-d-glucopyranosyl-l-ascorbic acid (AA-2ßG), ß-sitosterol, flavonoids and vitamins (in particular, riboflavin, thiamine, and ascorbic acid). LBPs are the primary active components of Lycium barbarum. In this review, we discuss the pharmacological activities of LBPs and other major components. They have been reported to mediate significant anti-aging effects, through antioxidant, immunoregulative, anti-apoptotic activities and reducing DNA damage. Thus, the basic scientific evidence for anti-aging effects of LBPs is already available. However, additional studies are needed to understand mechanisms by which LBPs mediate anti-aging properties. Novel findings from such studies would likely pave the way for the clinical application of traditional chinese medicine Lycium barbarum in modern evidence-based medicine. [ABSTRACT FROM AUTHOR]

Previous studies have shown that Lycium barbarum polysaccharides (LBPs) serve an important role in antioxidant activity to protect the cells and tissues. However, the specific mechanism of LBPs in the prevention of endometrial damage remains to be elucidated. Using morphological observation, cell proliferation assay, the detection of superoxide dismutase (SOD) activity and the content of malondialdehyde (MDA) in cell culture supernatant fluid, the detection by western blot analysis and reverse transcription-quantitative polymerase chain reaction of the mRNA and protein expression levels of caspase-3 and Bcl-2 in endometrial stromal cells (ESCs), it was demonstrated that, in vitro, hydrogen peroxide (H2O2)-induced death of ESCs, increased the content of MDA and decreased the activity of SOD, and decreased the expression of Bcl-2 and increased the expression of caspase-3. LBPs can inhibit H2O2-induced cell death of ESCs, decrease the content of MDA in ESCs and increase the activity of SOD, as well as increasing the expression of Bcl-2 and decreasing the expression levels of caspase-3. These findings suggested that LBPs can inhibit H2O2-induced apoptosis of EECs and that LBPs are able to offer a significant protection against oxidative stress to ESCs. [ABSTRACT FROM AUTHOR]

Abstract: Ethnopharmacological relevance: Lycium barbarum, a Solanaceous defoliated shrubbery, has been used as a kind of traditional Chinese herbal medicines for thousands of years. Lycium barbarum polysaccharide (LBP) is the main bioactive component of Lycium barbarum. The aim of this study was to investigate the radioresistant effect of LBP on the damage of male rats’ reproductive system and spermatogenic cells caused by low-dose 60Co-γ irradiation. Materials and methods: Male rats were randomly divided into 7 groups and treated with irradiation and/or LBP: normal control group, irradiation control group 1, irradiation control group 2, irradiation control group 3, LBP + irradiation group 1, LBP + irradiation group 2, and LBP + irradiation group 3. Results: It is found that mating function and testis organ coefficient in LBP + irradiation groups were significantly better than that of the corresponding irradiation control groups. LBP significantly up-regulates the expression of Bcl-2 while down-regulating the expression of Bax. And LBP also plays an important role in prevention mitochondrial membrane potential decrease. In addition, LBP can significantly reduce spermatogenic cells apoptosis. Conclusion: LBP has obvious protective effect on the male rats’ reproductive function and spermatogenic dysfunction induced by irradiation. [Copyright &y& Elsevier]

Lycium barbarum (L. barbarum) fruit or extract has been regarded as a superior-grade Chinese medicine, used to modulate body immunity and for anti-aging purposes. However, the underlying molecular mechanisms behind these effects remain unclear. In the present study, L. barbarum polysaccharides (LBPs), considered a major contributor of L. barbarum effects, were used to elucidate its mechanism of action by phenotypic and senescence associated-β-galactosidase (SA-β-gal) assays, evaluation of survival rates in vivo and expression profiling of genes related to the p53 signaling pathway in a zebrafish model. Zebrafish embryos were continuously exposed to various concentrations of LBPs (1.0, 2.0, 3.0 and 4.0 mg/ml) for 3 days. The results of fluorescent acridine orange and SA-β-gal staining indicated that cell apoptosis and senescence mainly occur in the head at 24 hours post fertilization (hpf) and 72 hpf. In addition, resistance to replicative senescence was observed at low doses of LBPs, especially at the 3.0 mg/ml concentration. Furthermore, the expression of genes that relate to aging, such as p53, p21 and Bax, was decreased, while that of Mdm2 and TERT genes was increased after treatment with LBPs. The results demonstrated that the effects of LBPs on cell apoptosis and aging might be mediated by the p53-mediated pathway. [ABSTRACT FROM AUTHOR]

Abstract: Polysaccharides were extracted from Lycium barbarum fruits in this work. Fourier transform infrared spectroscopy (FT-IR) and high-performance liquid chromatography (HPLC) have been employed to characterize this polysaccharides in the present study. The results of chemical composition indicated that the L. barbarum polysaccharides were composed of two kinds of monosaccharides, namely glucose and fructose in molar ratios of 1:2.1. The results indicated that the glucose and fructose were the predominant monosaccharides. IR spectrum of L. barbarum polysaccharides revealed a typical peaks of polysaccharides. The results still showed that L. barbarum polysaccharides significantly decreased the myocardium LD level, increased Na+–K+-ATPase and Ca2+-ATPase activities in heart ischemia reperfusion (IR) rats. In addition, L. barbarum polysaccharides still markedly decreased myocardium Bax positive rate and myocardial cell apoptosis and increased Bcl-2 positive rate in a dose-dependent manner. It may be concluded that administration of L. barbarum polysaccharides can prevented the development of cardiovascular diseases. [ABSTRACT FROM AUTHOR]

Lycium barbarum L., a classical traditional Chinese Medicine, has long been used to treat ocular diseases. Lycium barbarum polysaccharides (LBP) is an effective component of Lycium barbarum L. with a wide range of pharmacological activities. This research aims to investigate the inhibition of high glucose-induced angiogenesis by LBP in RF/6A cells. A high-glucose-induced angiogenesis model was established using monkey retinal vascular endothelial (RF/6A) cells. Different dosages administration times of LBP and glucose concentrations were tested. Under the optimized conditions, RF/6A cells were treated with LBP for 48 h, followed by another 48-h culture in high glucose (25 mmol/L) medium. The effect and mechanism of LBP were investigated following the treatment. The expression of miR-15a-5p and miR-15a-3p in RF/6A cells decreased significantly after 48 h of 25 or 50 mmol/L high glucose treatment. The expression of miR-15a-5p was higher than that of miR-15a-3p. Mimic-miR-15a-5p or 600 mg/L LBP could increase the apoptosis of cells and the total length of vascular branches. The expression of VEGFA, VEGFR2, and ANG2 proteins was reduced, while the expression of ANG1 protein was elevated. Expression of ASM mRNA and protein was also inhibited. LBP attenuates diabetic retinal angiogenesis by rescuing the expression of miR-15a-5p in RF/6A cells. [Display omitted] [ABSTRACT FROM AUTHOR]