Showing papers on "Salidroside published in 2023"

Mechanistic study of salidroside on ovalbumin-induced asthmatic model mice based on untargeted metabolomics analysis.

Abstract: Salidroside (SAL) is a natural component derived from Rhodiola rosea and is well known for its wide range of biological activities such as its anti-inflammatory and anti-oxidative properties. However, its effects and mechanisms of action related to asthma have not been well explored yet. Recent studies have found that changes in host metabolism are closely related to the progression of asthma. Many natural components can ameliorate asthma by affecting host metabolism. The use of untargeted metabolomics can allow for a better understanding of the metabolic regulatory mechanisms of herbs on asthma. This study aimed to demonstrate the anti-asthmatic effects and metabolic regulatory mechanisms of SAL. In this study, the therapeutic effects of SAL on asthmatic mice were tested at first. Secondly, the effects of SAL on the airway inflammatory reaction, oxidative stress, and airway remodeling were investigated. Finally, untargeted metabolomics analysis was used to explore the influence of SAL on lung metabolites. The results showed that SAL had a significant therapeutic effect on asthmatic model mice. Moreover, SAL treatment lowered interleukin (IL)-4, IL-5, and IL-13 levels but elevated interferon gamma (IFN-γ) and IL-10 levels in bronchoalveolar lavage fluid (BALF). Additionally, it also increased superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and decreased methane dicarboxylic aldehyde (MDA) levels in the lungs. Besides, SAL-treated mice showed decreased expression of smooth muscle actin (α-SMA), matrix metallopeptidase 2 (MMP2), matrix metallopeptidase 9 (MMP9), and transforming growth factor-beta 1 (TGF-β1) in the lung. Untargeted metabolomics analysis showed 31 metabolites in the lungs that were influenced by SAL. These metabolites were related to pyrimidine metabolism, steroid hormone biosynthesis, and tricarboxylic acid (TCA) cycle. In conclusion, SAL treatment can reduce the inflammatory response, oxidative stress, and airway remodeling in asthmatic model mice. The mechanism of SAL in the treatment of asthma may be related to the regulation of pyrimidine metabolism, steroid hormone biosynthesis, and the TCA cycle. Further studies can be carried out using targeted metabolomics and in vitro models to deeply elucidate the anti-inflammatory and anti-oxidative mechanisms of SAL on asthma based on regulating metabolism.

Complete Biosynthesis of Phenylethanoid Glycoside Verbascoside.

Abstract: Verbascoside, which was first discovered in 1963, is a well-known phenylethanoid glycoside (PhG) that exhibits antioxidant, anti-inflammatory, antimicrobial, and neuroprotective activities and contributes to the therapeutic effects of many medicinal plants. However, the biosynthetic pathway of verbascoside remains to be fully elucidated. Here, we report the identification of two missing enzymes in the verbascoside biosynthesis pathway by transcriptome mining and in vitro enzymatic assays. Specifically, a BAHD acyltransferase (hydroxycinnamoyl-CoA:salidroside hydroxycinnamoyltransferase [SHCT]) was shown to catalyze the regioselective acylation of salidroside to form osmanthuside A, and a CYP98 hydroxylase (osmanthuside B 3,3'-hydroxylase [OBH]) was shown to catalyze meta-hydroxylations of the p-coumaroyl and tyrosol moieties of osmanthuside B to complete the biosynthesis of verbascoside. Because SHCTs and OBHs are found in many Lamiales species that produce verbascoside, this pathway may be general. The findings from the study provide novel insights into the formation of caffeoyl and hydroxytyrosol moieties in natural product biosynthetic pathways. In addition, with the newly acquired enzymes, we achieved heterologous production of osmanthuside B, verbascoside, and ligupurpuroside B in Escherichia coli; this work lays a foundation for sustainable production of verbascoside and other PhGs in micro-organisms.

Salidroside attenuates oxygen and glucose deprivation-induced neuronal injury by inhibiting ferroptosis

Abstract: Objective: To evaluate the effect of salidroside on oxygen and glucose deprivation (OGD)-treated NT2 cells and its underlying mechanisms of action. Methods: Retinoic acid was used to induce the differentiation of NT2 cells into neurons. The effects of salidroside on survival, apoptosis, inflammatory response, and oxidative stress of neurons undergoing OGD were evaluated. Using precursor cells as controls, the effect of salidroside on the differentiation progression of OGD-treated cells was evaluated. In addition, the effect of erastin, a ferroptosis inducer, on NT2 cells was examined to investigate the underlying mechanisms of neuroprotective action of salidroside. Results: Salidroside alleviated the effects of OGD on neuronal survival, apoptosis, inflammation, and oxidative stress, and promoted NT2 cell differentiation. Moreover, salidroside prevented ferroptosis of OGD-treated cells, which was abolished following erastin treatment, indicating that ferroptosis mediated the regulatory pathway of salidroside. Conclusions: Salidroside attenuates OGD-induced neuronal injury by inhibiting ferroptosis and promotes neuronal differentiation.

Investigating the Effects and Mechanism of Rhodiola Rosea Injection on Cardiac Function in Rats with Chronic Heart Failure.

Abstract: AIM To study the effect of Rhodiola rosea injection on cardiac function and the reninangiotensin-aldosterone system (RASS) in rats with chronic heart failure. BACKGROUND Rhodiola rosea injection, a traditional Chinese medication for relieving blood stasis and improving blood circulation, is an excellent therapeutic for treating coronary heart diseaseangina pectoris. Rhodiola rosea injection's major component, salidroside, protects the cardiovascular system. But there isn't much first-hand evidence about how injectable Rhodiola rosea affects heart failure. OBJECTIVES In this study, a rat model of heart failure was established, and the effect of Rhodiola rosea injection on myocardial cell morphology, cardiac function, and ventricular remodelling in rats with heart failure was investigated. METHODS 66 SD male rats were selected; 10 were randomly selected as a blank control group, and 56 were treated intraperitoneally with doxorubicin (4 g/g). After 6 weeks, all animals had LVEF 60%. Established a heart failure model. Each group had 14 rats: model control, low-dose, mediumdose, and high-dose Rhodiola rosea injection. The 2mL/kg of Rhodiola rosea injection was injected into the tail vein once a day for 2 weeks. Both the blank and control groups received normal daily saline. After 2 weeks, the echocardiographic index, RASS-related index, and serum BNP level were assessed in all rats, and myocardial tissue morphology was observed. MiRNA423-5p, miRNA499-5p, and miRNA210-3p were extracted from peripheral blood. Rhodiola rosea injection on its expression was compared to healthy control rats. RESULTS 6 mL/kg Rhodiola rosea injection lowered LVEDV and LVESV while increasing LVEF and LVFS. Injections of 6 mL/kg Rhodiola rosea reduce plasma levels of miR-210-3p, miR-423- 5p, miRNA-499, and BNP in heart failure model rats. The 6 mL/kg Rhodiola rosea injection can restore the RASS indexes of heart failure rats to the level of the normal group. CONCLUSION The present study offers preliminary evidence supporting the use of Rhodiola rosea injection in the treatment of heart failure and offers a solid foundation for clinical off-label medication use.

Salidroside facilitates therapeutic angiogenesis in diabetic hindlimb ischemia by inhibiting ferroptosis.

Abstract: Hindlimb ischemia (HLI), in which blood perfusion to the hindlimb is obstructed, is one of the major complications of diabetes. Skeletal muscle cells are crucial for revascularization as they can secrete various angiogenic factors; however, hyperglycemia impairs their viability and subsequently their angiogenic potential. Salidroside can promote skeletal muscle cell viability under hyperglycemia; however, the molecular mechanism is still poorly understood. Here we revealed that salidroside could suppress hyperglycemia-induced ferroptosis in skeletal muscle cells by promoting GPX4 expression, thereby restoring their viability and paracrine functions. These in turn promoted the proliferation and migration potentials of blood vessel-forming cells. Furthermore, we showed that salidroside/GPX4-mediated ferroptosis inhibition is crucial for promoting angiogenesis and blood perfusion recovery in diabetic HLI mice. Together, we reveal a novel molecular mechanism of salidroside in enhancing skeletal muscle cells-mediated revascularization and blood perfusion recovery in diabetic HLI mice, further highlighting it as a potential compound for treating diabetic HLI.

Salidroside protects against intestinal barrier dysfunction in septic mice by regulating IL‑17 to block the NF‑κB and p38 MAPK signaling pathways

Abstract: Sepsis is a systemic inflammatory response syndrome, mainly caused by infection or suspected infectious factors. The intestine is not only one of the most easily involved organs in the course of sepsis, but also the dynamic organ for the course of sepsis. The present study investigated the protective effect and mechanism of salidroside on intestinal barrier dysfunction of septic mice. Briefly, C57BL/6 mice were used to establish a septic model and then administered with salidroside. The ileum tissues of mice were examined by histopathological examination. Fluorescein isothiocyanate-dextran concentration was measured. IL-17, IL-6, IL-13 and TNF-α levels in ileum tissues and NF-κB and p38 MAPK activations were detected by ELISA and the expressions of NF-κB p65 and p38 MAPK protein with their phosphorylation and intestinal tight junction proteins were gauged by western blotting. The above assays were performed again to investigate the effect of anti-IL-17A and salidroside (160 mg/kg) alone or in combination. The septic model induced the ileum tissue injury, increased intestinal permeability and TNF-α, IL-17 and IL-6 levels, activated NF-κB and p38 MAPK pathways, promoted the expressions of NF-κB p65 and p38 MAPK and their phosphorylation, while suppressing the levels of IL-13 and intestinal tight junction proteins. Salidroside and anti-IL-17A partially reversed the above effects of septic model, which in combination further strengthened the reversing effect. Collectively, salidroside protected against intestinal barrier dysfunction in septic mice by downregulating IL-17 level to inhibit NF-κB and p38 MAPK signaling pathways, thus providing a new treatment direction.

Brain Network Homeostasis and Plasticity of Salidroside for Achieving Neuroprotection and Treating Psychiatric Sequelae Stemming from Stress

Abstract: Abstract The coronavirus disease 2019 (COVID-19) pandemic has affected the mental health of individuals worldwide, and the risk of psychiatric sequelae and consequent mental disorders has increased among the general population, health care workers and patients with COVID-19. Achieving effective and widespread prevention of pandemic-related psychiatric sequelae to protect the mental health of the global population is a serious challenge. Salidroside, as a natural agent, has substantial pharmacological activity and health effects, exerts obvious neuroprotective effects, and may be effective in preventing and treating psychiatric sequelae and mental disorders resulting from stress stemming from the COVID-19 pandemic. Herein, we systematically summarise, analyse and discuss the therapeutic effects of salidroside in the prevention and treatment of psychiatric sequelae as well as its roles in preventing the progression of mental disorders, and fully clarify the potential of salidroside as a widely applicable agent for preventing mental disorders caused by stress; the mechanisms underlying the potential protective effects of salidroside are involved in the regulation of the oxidative stress, neuroinflammation, neural regeneration and cell apoptosis in the brain, the network homeostasis of neurotransmission, HPA axis and cholinergic system, and the improvement of synaptic plasticity. Notably, this review innovatively proposes that salidroside is a potential agent for treating stress-induced health issues during the COVID-19 pandemic and provides scientific evidence and a theoretical basis for the use of natural products to combat the current mental health crisis.

Neuroprotective effects of salidroside against 6-OHDA-induced oxidative stress in PC12 cells

Abstract: Neuroprotective effects of salidroside (Sal) in PC12 cells against oxidative stress induced by 6-hydroxydopamine (6-OHDA). Sal scavenges reactive oxygen species (ROS), enhances antioxidant enzyme activity (SOD, CAT, GPX4), and reduces α-synuclein (α-syn) accumulation.

Salidroside attenuates LPS-induced kidney injury through activation of SIRT1/Nrf2 pathway.

Abstract: BACKGROUND Salidroside (SAL) is an anti-inflammatory, antioxidant, anticancer, neuroprotective, and renal protective active ingredient extracted from the Chinese herb. Rhodiola Rosea. However, the role of SAL in kidney injury has not yet been elucidated. The study investigates SAL's protective effect and mechanism in lipopolysaccharide (LPS)-induced kidney injury. METHODS Male C57BL/6 wild-type mice (6-8 weeks old) were intraperitoneally injected with 10 mg/kg LPS for 24 h and SAL (50 mg/kg) 2 h before the LPS injection. Biochemical and TUNNEL staining assay analyses were carried out to assess kidney injury. The Elisa assay analyzed the mRNA expression of NGAL and KIM-1. RT-qPCR and Western blotting measured the mRNA and protein expression of HO-1, NQO1, Beclin1, P62, SIRT1, Nrf2, and PNCA, respectively. RESULTS Our study found that mice co-treated with SAL had significantly reduced blood urea nitrogen (BUN), serum creatinine (Scr), neutrophil gelatinase-associated lipocalin (NGAL), and kidney injury molecule-1 (KIM-1) levels in serum of LPS-induced mice. SAL cotreatment potentially decreased the apoptosis rate of kidney tissue and podocytes induced by LPS. SAL significantly reduced the content of malondialdehyde (MDA) and increased superoxide dismutase (SOD) in LPS-treated mice. Autophagy-related proteins Beclin-1 increased but decreased P62 protein expression by cotreatment of SAL in LPS-injected mice. SAL enhanced the Sirtuin 1 (SIRT1) and nuclear factor erythroid 2-related factor 2 (Nrf2) protein expression in LPS-induced kidney tissues. CONCLUSION Our results speculate that SAL protects against LPS-induced kidney injury through activation of the SIRT1/Nrf2 pathway.

The Use of Reference Materials In the Analysis of Medicinal Plant Raw Materials and Herbal Medicinal Products

Abstract: The need to improve pharmacopoeial approaches to the standardization of medicinal plant raw materials (MPRMs) and herbal medicinal products (HMPs), and the need to ensure the implementation of the principle of «cross-cutting» standardization in the series «medicinal plant raw material – phyto-substance – herbal medicinal product» determine the relevance of developing new, more rational approaches to the analysis of objects of plant origin.The purpose of the research was the theoretical and experimental substantiation of the use of reference materials in the development of assay procedures on the example of certain types of plant raw materials and products based on it from the standpoint of the chemical composition, stability and physicochemical properties of the biologically active compounds contained in them.Assay of active substances was carried out by high performance liquid chromatography (HPLC) using a Milichrome-6 chromatograph with a spectrophotometric detector in the ultraviolet (UV-) region. The UV spectra were recorded using a Specord 40 spectrophotometer. The measurement results were processed using the WinASPECT and Microsoft Excel 2016 programs.As a result of research, procedures for assay of syringin in the bark of Syringa vulgaris, and in the rhizomes and roots of Eleutherococcus senticosus, rosavin and salidroside in the rhizomes and roots of Rhodiola rosea, arbutin in the leaves of Arctostaphylos uva-ursi and Vaccinium vitis-idaea, isosalipurposide in the flowers of Helichrysum arenarium, the amount of anthracene derivatives in fresh leaves of Aloe arborescens were developed and validated. Spectrophotometric methods for determining the amount of biologically active phenylpropanoids in terms of eleutheroside B (syringin) in MPRMs and HMPs of Eleutherococcus senticosus and the amount of aralosides in the roots of Aralia Manchurian were introduced. Based on the data obtained, the scientific rationale for the use of reference materials of syringin (Syringa vulgaris bark, Eleutherococcus senticosus rhizomes and roots), rosavin and salidroside (Rhodiola rosea rhizomes and roots), the sum of ammonium salts of aralosides (Manchurian aralia root), arbutin (Arctostaphylos uva-ursi and Vaccinium vitis-idaea leaves), mixtures of aloins A and B (Aloe arborescens fresh leaves) in the analysis procedures was provided. The concept of a systematic approach to the analysis of medicinal plant raw materials and products based on it was formulated.

Biomimetic tri-layered small-diameter vascular grafts with decellularized extracellular matrix promoting vascular regeneration and inhibiting thrombosis with the salidroside

Abstract: Small-diameter vascular grafts (SDVGs) are urgently required for clinical applications. Constructing vascular grafts mimicking the defining features of native arteries is a promising strategy. Here, we constructed a tri-layered vascular graft with a native artery decellularized extracellular matrix (dECM) mimicking the component of arteries. The porcine thoracic aorta was decellularized and milled into dECM powders from the differential layers. The intima and media dECM powders were blended with poly (l-lactide-co-caprolactone) (PLCL) as the inner and middle layers of electrospun vascular grafts, respectively. Pure PLCL was electrospun as a strengthening sheath for the outer layer. Salidroside was loaded into the inner layer of vascular grafts to inhibit thrombus formation. In vitro studies demonstrated that dECM provided a bioactive milieu for human umbilical vein endothelial cell (HUVEC) extension adhesion, proliferation, migration, and tube-forming. The in vivo studies showed that the addition of dECM could promote endothelialization, smooth muscle regeneration, and extracellular matrix deposition. The salidroside could inhibit thrombosis. Our study mimicked the component of the native artery and combined it with the advantages of synthetic polymer and dECM which provided a promising strategy for the design and construction of SDVGs.

Geraniol-Derived Monoterpenoid Glucosides from Rhodiola rosea: Resolving Structures by QM-HifSA Methodology.

Abstract: Monoterpenoids are integral to the chemical composition of the widely used adaptogenic dietary supplement Rhodiola rosea. The present study expands the chemical space and stereochemical information about these taxon-specific constituents from the isolation and characterization of five geraniol-derived glucosides, 1-5. While 1 and 2 exhibited almost identical NMR spectra and shared the same 2D structure ascribed to the 4-hydroxygeraniolglucoside previously described as rosiridin, the NMR-based Mosher ester method revealed the enantiomeric nature of their aglycone moieties. This marks the first report of enantiomeric aglycones among geraniol derivatives. These findings also resolve the long-standing dispute regarding the absolute configuration of rosiridin and congeneric C-4 hydroxylated geraniols and may help explain incongruent bioactivity reports of R. rosea extract. Moreover, the three previously undescribed geranioloids 3-5 were fully characterized by extensive spectroscopic analysis. Quantum mechanics-driven 1H iterative functionalized spin analysis (QM-HifSA) was performed for all isolates and provides detailed NMR spin parameters, with adequate decimal place precision, which enable the distinction of such close congeners exhibiting near identical NMR spectra with high specificity. The outcomes also reinforce the importance of reporting chemical shifts and coupling constants with adequate decimal place precision as a means of achieving specificity and reproducibility in structural analysis.

Salidroside Attenuates Cisplatin-Induced Ototoxicity: An Experimental Study In Vitro and In Vivo

Abstract: Oxidative damage to hair cells is the major cause of ototoxicity induced by cisplatin (cis)-based chemotherapy. In this study, we aimed to assess how salidroside (SAL) protected cochlear explants (CEs) and HEI-OC1 cell lines against cis-induced ototoxicity and reduced relative hearing loss in mouse models. Furthermore, the protective mechanism of the Nrf2/ARE pathway was investigated. Cell Counting Kit-8 was used to measure the viability of HEI-OC1 cells. Flow cytometry and the TUNEL assay were used to evaluate cell apoptosis. Flow cytometry was used to measure intracellular reactive oxygen species (ROS). Immunofluorescence staining determined the changes in mitochondrial membrane potential (ΔΨm). Western blot was used to measure the levels of caspase-3 and Nrf-2. An analysis of Nrf2 and target gene levels of expression was conducted using qRT-PCR. Hearing was monitored using auditory brainstem response audiometry. In cochlear explants, SAL inhibits cis-induced apoptosis of HEI-OC1 cells and decreased hair cell apoptosis. SAL inhibited cis-induced apoptosis by lowering intracellular ROS, preserving mitochondrial function, and reducing caspase-3 expression. Moreover, auditory cells were protected from the toxic effects of cis by the Nrf2-ARE pathway after treatment with SAL. In Vivo, SAL could protect against cis-induced hearing loss, and the use of the PLGA-poloxamer nanohydrogel as a carrier increased the protection efficiency of SAL. Through its ability to reduce oxidative stress, SAL could protect auditory cell lines from cis-induced apoptosis In Vitro and attenuate cis-induced hearing loss In Vivo. Nano-based drug delivery can improve the protection efficiency of SAL. Further research should be conducted on the antioxidant capacity of SAL and its use in ototoxicity.

Salidroside alleviates acetaminophen-induced hepatotoxicity via Sirt1-mediated activation of Akt/Nrf2 pathway and suppression of NF-κB/NLRP3 inflammasome axis.

Abstract: Acetaminophen (APAP) overdose-induced hepatotoxicity is the most common cause of drug-induced liver injury worldwide, which is significantly linked to oxidative stress and sterile inflammation. Salidroside is the main active component extracted from Rhodiola rosea L., with anti-oxidative and anti-inflammatory activities. Herein, we investigated the protective effects of salidroside on APAP-induced liver injury and its underlying mechanisms. Pretreatment with salidroside reversed the impacts of APAP on cell viability, LDH release, and cell apoptosis in L02 cells. Moreover, the phenomena of ROS accumulation and MMP collapse caused by APAP were reverted by salidroside. Salidroside elevated the levels of nuclear Nrf2, HO-1, and NQO1. Using PI3k/Akt inhibitor LY294002 further confirmed that salidroside mediated the Nrf2 nuclear translocation through the Akt pathway. Pretreatment with Nrf2 siRNA or LY294002 markedly prevented the anti-apoptotic effect of salidroside. Additionally, salidroside reduced the levels of nuclear NF-κB, NLRP3, ASC, cleaved caspase-1, and mature IL-1β elevated by APAP. Moreover, salidroside pretreatment increased Sirt1 expression, whereas Sirt1 knock-down diminished the protective activities of salidroside, simultaneously reversing the up-regulation of the Akt/Nrf2 pathway and the down-regulation of NF-κB/NLRP3 inflammasome axis mediated by salidroside. We then used C57BL/6 mice to establish APAP-induced liver injury models and found that salidroside significantly alleviated liver injury. Furthermore, western blot analyses showed that salidroside promoted the Sirt1 expression, activated the Akt/Nrf2 pathway, and inhibited the NF-κB/NLRP3 inflammasome axis in APAP-treated mice. The findings of this study support a possible application of salidroside in the amelioration of APAP-induced hepatotoxicity.

Highly Efficient Biosynthesis of Salidroside by a UDP-glucosyltransferase-catalyzed Cascade Reaction

Abstract: Abstract Objective Salidroside is an important plant-derived aromatic compound with diverse biological properties. The main objective of this study was to synthesize salidroside from tyrosol using UDP-glucosyltransferase (UGT) with in situ regeneration of UDP-glucose (UDPG). Results The UDP-glucosyltransferase 85A1 (UGT85A1) from Arabidopsis thaliana ,which showed high activity and regioselectivity towards tyrosol, was selected for the production of salidroside. Then, an in vitro cascade reaction for in situ regeneration of UDPG was constructed by coupling UGT85A1 to sucrose synthase from Glycine max ( Gm SuSy). The optimal UGT85A1- Gm SuSy activity ratio of 1:2 was determined to balance the efficiency of salidroside production and UDP-glucose regeneration. Different cascade reaction conditions for salidroside production were also determined. Under the optimized condition, salidroside was produced at a titer of 6.0 g/L with a corresponding molar conversion of 99.6% and a specific productivity of 199.1 mg/L/h in a continuous feeding reactor. Conclusion This is the highest salidroside titer ever reported so far using biocatalytic approach.

Salidroside restores glucocorticoid sensitivity in chronic obstructive pulmonary disease by activating Nrf2/HO-1 pathway

Abstract: Corticosteroid resistance is the essential obstacle for effective treatment of chronic obstructive pulmonary disease (COPD). Oxidative stress and persistent chronic inflammation caused by cigarette smoke are likely to induce this corticosteroid insensitivity. Salidroside (Sal) is a main ingredient of traditional Chinese medicine rhodiola, which has the effects of anti-oxidation and anti-inflammatory. We aimed to investigate the role of Sal in the corticosteroid sensitivity of COPD. Collecting peripheral blood mononuclear cells (PBMC) from healthy volunteers (HV) and patients with COPD, and human monocytic U937 cells stimulated by normal culture and cigarette smoke extract (CSE), corticosteroid sensitivity was determined as the dexamethasone concentration causing 30% inhibition of tumor necrosis factor alpha (TNF-α)-induced IL-8 production (Dex-IC ) in these cells. Compared with PBMC from HV and normally cultured U937, in PBMC from COPD patients and U937 cells stimulated by CSE, the inhibitory effect of dexamethasone on IL-8 was weakened and the levels of nuclear factor erythroid 2‐related factor 2 (Nrf2) and histone deacetylase‐2 (HDAC2) was reduced. In conclusion, Sal restored dexamethasone inhibition of IL‐8 production, accompanied by raising the expression of Nrf2 and HDAC2 levels. Sal may upregulate HDAC2 expression by activating the Nrf2/HO-1 signaling pathway, and then restore corticosteroid sensitivity in COPD.

Salidroside ameliorates memory impairment following long-term ethanol intake in rats by modulating the altered intestinal microbiota content and hippocampal gene expression

Abstract: Background Salidroside (Sal), the main component of a famous herb Rhodiola rosea L, enhances memory performance and reduces fatigue. Therefore, this study assessed the effect of Sal on memory impairment induced by a long-term intake of ethanol (EtOH) in rats and investigated its relevant mechanisms using gut microbiota metagenomic analysis and hippocampal transcriptomic analysis. Methods Eighteen male SD rats were divided into the normal control group (CON group), EtOH model group (Model group), and Sal treatment group (Sal group). The rats in the Model and Sal groups intragastrically (i.g.) received 2 g/kg EtOH for 30 consecutive days, whereas the CON group was given an equal volume of distilled water. Meanwhile, the rats in the Sal group were administered i.g. 30 mg/kg Sal 60 min after EtOH intake. All rats were tested in the eight-arm maze for their memory function every 3 days. On the 30th day, metagenomic analyses of gut microbiota and transcriptomic analyses of the hippocampus were performed. Results Compared with the Model group, Sal treatment reduced the total time to complete the eight-arm maze task, decreased the number of arm entries, and abated the working memory error that was significant from the 9th day. Additionally, Sal intervention improved the gut microbiota composition, such as the increased abundance of Actinobacteria and Bifidobacterium, which was related to the metabolism of amino acids and terpenoid carbohydrate, endocrine function, and signal transduction by neurotransmitters. In the hippocampus, the EtOH intake differentially expressed 68 genes (54 genes increased, whereas 14 genes decreased), compared with the CON group, whereas Sal intervention affected these changes: 15 genes increased whereas 11 genes decreased. And, enrichment analyses revealed these genes were related to the structural components of the ribosome, mRNA splicing process, protein translation, mitochondria function, and immunological reaction. Finally, a correlation analysis found the memory impairment was positively correlated with the abnormal upregulation of Tomm7 but negatively correlated with decreased abundance of gut Alistipes_indistinctus, Lactobacillus_taiwanensis, Lactobacillus_paragasseri, and Lactobacillus johnsonii. Conclusion Sal improved memory impairment caused by long-term EtOH intake in rats, which may be related to its regulation of gut dysbiosis and hippocampal dysfunction.

Retraction: Insulin receptor A and Sirtuin 1 synergistically improve learning and spatial memory following chronic salidroside treatment during hypoxia

Abstract: The above article from the Journal of Neurochemistry, published online on 14 July 2015 in Wiley Online Library (wileyonlinelibrary.com), and in Volume 135, pp. 332–346, has been retracted by agreement between the authors, Kalpana Barhwal, Saroj K. Das, Ashish Kumar, Sunil K. Hota, Ravi B. Srivastava, and John Wiley and Sons Ltd. The retraction has been agreed upon concerns raised by a third party following the admission of Sunil K. Hota that this article contained data that cannot be retrieved and verified. During the investigation, several inconsistencies were found. In Figure 4a, the two bands in the red boxed areas appeared similar, and there was unexpected placement of top bands with respect to the lower smears, and a sharp vertical transition between lanes. In Figure 4b and 4d, similarities were observed between the boxed areas highlighted in the same color. In Figure 5a, the immunoblots appeared to have repeated features. In Figure 6a, repetitive patterns were observed in the bottom right panel. In Figure 6b, the lanes appeared similar in the GADPH panel. These issues called the conclusions of the manuscript into question. Accordingly, the conclusions of this manuscript are considered substantially compromised.