Biomedical subjects

Liang Xiao

Publications and source records attributed to Liang Xiao.

14 recordsLinked to original sources

PubMed2026

Alleviation of allergic rhinitis symptoms in an animal model by Lactiplantibacillus plantarum BGI-N6.

Allergic rhinitis (AR) is a chronic inflammatory disease with rising global prevalence and a substantial public health burden. Current treatments have limited efficacy and tolerability, highlighting the need for new strategies. Probiotics represent a promising approach due to their ability to modulate gut microbiota and host immunity. Here, we investigated the preventive potential of Lactiplantibacillus plantarum BGI-N6 in an OVA/ALUM-induced AR rat model. BGI-N6 administration alleviated AR symptoms and nasal mucosal pathology, reduced key allergic mediators, shifted serum immunoglobulin and cytokine levels toward normal, and restored the Th1/Th2/Th17/Treg balance. Metagenomic sequencing of cecal contents showed that these effects were accompanied by expansion of Bacteroidota-affiliated SCFA-producing taxa, restoration of microbial functional capacity, and identification of 41 core functional genes (KEGG Orthologues) consistently shifted across all three dose groups, with Bacteroides showing the strongest enrichment. Correlation analyses further connected these microbial shifts with immune parameters. These findings support BGI-N6 as a probiotic intervention for AR and implicate gut microbiota remodeling as a central correlate of probiotic-induced immunomodulation.

Animals↗

PubMed2006

Involvement of multitargets in paeoniflorin-induced preconditioning.

Paeoniflorin (PF) is the principal component of Paeoniae radix prescribed in traditional Chinese medicine. The delayed neuroprotection induced by PF preconditioning and its underlying mechanisms were investigated in rat middle cerebral artery occlusion (MCAO) and reperfusion model. At a dosage of 20 or 40 mg/kg, PF preconditioning 48 h before MCAO followed by 24-h reperfusion significantly reduced the mortality and infarct volume and reversed the neurological deficits caused by ischemia. Likewise, the ameliorative effects on mortality, infarct size, and neurological impairment induced by MCAO emerged as well when PF was administered 24 h, 48 h, or 5 days before MCAO at the dose of 20 mg/kg. Furthermore, comparative proteomics analysis was adopted to identify the differentially expressed proteins induced by PF preconditioning itself. The relative levels of 42 proteins were altered after PF preconditioning, among which 20 were elevated and 22 reduced. In summary, A(1) receptor-regulator of G protein signaling-K(ATP) signaling, arachidonic acid cascade, nitric oxide system, markers of neuronal damage, mitochondrial damage-related molecules, and the mitogen-activated protein kinase and nuclear factor-kappaB pathway are associated with the mechanisms of PF preconditioning.

Adenosine Triphosphate↗

PubMed2006

Paeoniflorin attenuates chronic cerebral hypoperfusion-induced learning dysfunction and brain damage in rats.

Chronic cerebral hypoperfusion, a mild ischemic condition, is associated with the cognitive deficits of AD. Paeoniflorin (PF), a major constituent of peony root, was proved to be neuroprotective in middle cerebral artery occlusion model. In this study, we investigated whether PF could attenuate chronic cerebral hypoperfusion-induced learning dysfunction and brain damage in rat. Seven weeks after permanent bilateral occlusion of the common carotid arteries, the rats were tested in the Morris water maze. Subsequently, the animals were sacrificed and neurons, astrocytes and microglias were labeled with immunocytochemistry in hippocampus. PF at the dose of 2.5 mg/kg ameliorated cerebral hypoperfusion-related learning dysfunction and prevented CA1 neuron damage. Chronic cerebral hypoperfusion increased the immunoreactivity of astrocytes and microglias in hippocampus. The increase was prevented by PF at the dose of 2.5 mg/kg. Cerebral hypoperfusion also increased expression of nuclear factor-kappaB (NF-kappaB), mostly in astrocytes, but not in neurons. With the treatment of PF (2.5 mg/kg), NF-kappaB immunostaining was diminished in hippocampus. Our results demonstrated that PF could attenuate cognitive deficit and brain damage induced by chronic cerebral hypoperfusion and that suppression of neuroinflammatory reaction in brain might be involved in PF-induced neuroprotection.

Animals↗

PubMed2006

Determination of ionic conductivity and its impact on proton diffusion model for nickel hydroxide.

The ionic conductivity is an important but previously ignored aspect for the nickel hydroxide used in alkaline batteries. With a specially designed device, the ionic conductivity is determined for single beads of spherical nickel hydroxide in KOH solutions. The apparent ionic conductivity is found on the order of 10(-3)-10(-2) S cm-1 in 6 M KOH and to change with the conductivity of the solution in which the bead is immersed. The ionic conductivity of the bead can be mainly attributed to the electrolyte absorbed in the bead. On the basis of these findings, the dual structure model for proton diffusion in spherical nickel hydroxide is refined by specifying nanoparticles to be the component showing a large apparent proton diffusion coefficient (on the order of 10(-7) cm2 s-1). This refined model is able to interpret the main features of the diffusion coefficients reported in the literature, including the unusually large scattering (up to 6 orders of magnitude) and inconsistency in the dependence of proton diffusion coefficient on the state of the charge. Besides, this refined model is supported by the influence of bulk KOH concentration on chronoamperometry and transmission electron microscopy observations.

Journal Article↗

PubMed2006

Vip3A is responsible for the potency of Bacillus thuringiensis 9816C culture supernatant against Helicoverpa armigera and Spodoptera exigua.

Culture supernatant of Bacillus thuringiensis 9816C had high toxicity against Helicoverpa armigera and Spodoptera exigua. However, it lost insecticidal activities after being bathed in boiling water for 5 min. Acrystalliferous mutants of Bt9816C (Bt9816C-NP1 and Bt9816C-NP2) cured of its endogenous plasmids no longer possessed vip3A gene and toxicity. The 89 kD protein which existed in Bt9816C supernatant disappeared in the two mutants' supernatant; nevertheless, the two mutants still exhibited hemolytic and phospholipase C activity as Bt9816C did. The vip3A gene of Bt9816C, vip3Aa18, was cloned and expressed in Escherichia coli BL21. Bioassay demonstrated that the recombinant E. coli had high toxicity against S. exigua. Taken together, it suggested that Vip3A protein was responsible for the toxicity of Bt9816C culture supernatants.

Animals↗

PubMed2005

Effects of paeoniflorin on the cerebral infarction, behavioral and cognitive impairments at the chronic stage of transient middle cerebral artery occlusion in rats.

In the present study, the effects of paeoniflorin (PF), a characteristic monoterpene glucoside isolated from Paeoniae Radix, on cerebral infarction, neurological symptoms, tongue protrusion (TP) and performance in the water maze were examined at the chronic stage (4 weeks) of transient cerebral ischemia using a rat middle cerebral artery occlusion (MCAO) model. One-day (10 mg/kg, twice, s.c.) or seven-day (2.5-10 mg/kg, twice a day, s.c.) injection of PF significantly reduced the infarct volume as well as ameliorated the deficits in neurological symptoms caused by transient MCAO at chronic stage. Transient MCAO also induced impairments in TP and performance in the water maze. Treatment with PF was able to reverse or alleviate these impairments. These results indicate that PF may be effective for treatment of stroke.

Animals↗

PubMed2005

Proton diffusion determination and dual structure model for nickel hydroxide based on potential step measurements on single spherical beads.

Potential step measurement is carried out on single beads of spherical nickel hydroxide to determine the proton diffusion coefficient (D) and concentration of the effective proton vacancies (C). The semi-infinite diffusion equation for the initial stage and the finite diffusion equation for the long-term of the current response to potential step are used for deducing the D and C values. The diffusion coefficients deduced from short and long-term current responses are in the order of magnitude 10(-7) and 10(-10) cm2 s(-1), respectively. The sum of the effective proton vacancy concentrations associated with the two D values comes out to be equal within experimental error to the effective proton vacancy concentration converted from the released electricity during discharge. A dual structure model is proposed to interpret the above-mentioned findings, featuring densely packed grains within which proton diffusion is slow and an inter-grain matrix where proton diffusion is fast. With this model the huge difference (about 6 orders of magnitude) in D values reported in the literature as well as the controversy of the dependence of diffusion coefficient on the state of charge can be largely rationalized. This dual structure model is supported by SEM and AFM observations.

Journal Article↗

PubMed2005

Down regulation of cyclooxygenase-2 is involved in delayed neuroprotection by ischemic preconditioning in rats.

AIM: To examine whether the prostaglandins (PGs) pathway is involved in triggering delayed neuroprotection by ischemic preconditioning (IPC) and evaluate the effects of IPC on cyclooxygenase-2 (COX-2) expression following focal cerebral ischemia and reperfusion in rats. METHODS: IPC was induced by 10 min of saline infusion into the left internal carotid artery with the right common carotid artery clamped at the same time. Middle cerebral artery occlusion (MCAO) and reperfusion model was produced using intraluminal filament method. RESULTS: IPC 48 h prior to MCAO significantly reduced infarct area as compared with MCAO alone. A nonselective inhibitor of COX indomethacin (3 mg/kg, ip) applied 1 h prior to or 1 h after IPC failed to affect its protective effects. IPC had no direct effect on the cortex COX-2 mRNA and protein expression 72 h later, but decreased the expression of COX-2 mRNA and protein following ischemia and reperfusion insult. CONCLUSION: PGs pathways was not involved in triggering delayed neuroprotection by IPC, and IPC induced down-regulation of COX-2 following focal cerebral ischemia and reperfusion in rats in vivo.

Animals↗

PubMed2003

Involvement of capsaicin-sensitive sensory nerves in cardioprotection of rutaecarpine in rats.

In the present study, we examined whether rutaecarpine protects against myocardial ischemia-reperfusion injury in rats and whether the protective effects of rutaecarpine are related to activation of capsaicin-sensitive sensory nerves. Rats were pretreated with rutaecarpine 10 min before the experiment, and then the left main coronary artery of rat hearts was subjected to 60-min occlusion followed by 3-h reperfusion. The infarct size, serum concentration of creatine kinase, and CGRP concentration in plasma were measured. Pretreatment with rutaecarpine (100 or 300 microg/kg, i.v.) significantly reduced infarct size and creatine kinase release concomitantly with a significant increase in plasma concentrations of CGRP. These effects of rutaecarpine were completely abolished by capsazepine (38 mg/kg, s.c.), a competitive vanilloid receptor antagonist, or by pretreatment with capsaicin (50 mg/kg, s.c.), which selectively depletes transmitters in capsaicin-sensitive sensory nerves. These results suggest that rutaecarpine protects against myocardial ischemia-reperfusion injury in rats and that the protective effects of rutaecarpine are related to activation of capsaicin-sensitive sensory nerves via activating vanilloid receptors.

Alkaloids↗

PubMed2003

The depressor and vasodilator effects of rutaecarpine are mediated by calcitonin gene-related peptide.

Previous studies have shown that rutaecarpine has depressor and vasodilator effects, and activates vanilloid receptors to evoke calcitonin gene-related peptide (CGRP) release. In the present study, we examined whether the depressor and vasodilator effects of rutaecarpine are related to the stimulation of endogenous CGRP release via activation of vanilloid receptors in rats. Rutaecarpine (30, 100, or 300 microg/kg, i. v.) caused a depressor effect concomitantly with an increase in the plasma concentrations of CGRP in a dose-dependent manner, and the effects of rutaecarpine were abolished by pretreatment with capsaicin (50 mg/kg, s. c.) which depletes neurotransmitters in sensory nerves. In aortic and superior mesenteric arterial rings, rutaecarpine (10 (-7)-10(-5) M) or capsaicin (3 x 10(-9)-3 x 10(-6) M) caused a concentration-dependent vasodilator response, which was significantly attenuated by capsazepine (10(-5) M), a competitive vanilloid receptor antagonist, or by CGRP-(8-37) (10(-6) M), a selective CGRP receptor antagonist. After pretreatment with capsaicin (10(-5) M) for 20 min, vasodilator responses to rutaecarpine were also markedly attenuated. Similarly, pretreatment with rutaecarpine (10(-5) M) for 20 min also attenuated vasodilator responses to capsaicin. These results suggest that the depressor and vasodilator effects of rutaecarpine are related to stimulation of endogenous CGRP release via activation of vanilloid receptors in rats.

Alkaloids↗

PubMed2002

Effect of age on alpha-calcitonin gene-related peptide-mediated delayed cardioprotection induced by intestinal preconditioning in rats.

In the present study, we examined whether age-related reduction in cardioprotection of intestinal ischemic preconditioning is related to stimulation of the release and synthesis of calcitonin gene-related peptide (CGRP) in rats. Ischemia-reperfusion injury was induced by a 45-min coronary artery occlusion and 180-min reperfusion, and ischemic preconditioning was induced by six cycles of 4-min ischemia and 4-min reperfusion of the small intestine. The serum concentration of creatine kinase, infarct size, the expression of CGRP isoforms (alpha- and beta-CGRP) mRNA in lumbar dorsal root ganglia and CGRP concentration in plasma were measured. Pretreatment with intestinal ischemic preconditioning for 24 h significantly reduced infarct size and creatine kinase release concomitantly with a significant increase in the expression of alpha-CGRP mRNA, but not beta-CGRP mRNA, and plasma concentrations of CGRP at 6 months of age but not at 24 months of age. These results suggest that the delayed cardioprotective effect of intestinal ischemic preconditioning is decreased in senescent rats, and the age-related change is related to reduction of the synthesis and release of alpha-CGRP.

Age Factors↗

PubMed2002

Heme oxygenase-1 pathway is involved in delayed protection induced by heat stress against cardiac ischemia-reperfusion injury.

Previous studies have shown that heme oxygenase-1 (HO-1), a heat stress protein (HSP32), has a beneficial effect on the ischemic myocardium. The purpose of the present study was to explore whether HO-1 is involved in delayed cardioprotection provided by heat stress in vivo. Sprague--Dawley rats were pretreated with whole body hyperthermia (rectal 42 degrees C) for 15 min followed by ischemia-reperfusion 24 h later. Ischemia-reperfusion injury was induced by 45 min of coronary artery occlusion followed by a 3-h reperfusion. Myocardial injury degree was evaluated by measurement of infarct size and serum creatine kinase (CK) activity. The expression of HO-1 mRNA and protein in myocardial tissues were measured. Pretreatment with hyperthemia significantly reduced infarct size and CK release during reperfusion, which was completely blocked by pretreatment with ZnPP-9, an inhibitor of HO and methylene blue, an inhibitor of soluble guanylate cyclase. Heat stress also significantly increased the expression of HO-1 mRNA and protein, and the effect was not affected by pretreatment with methylene blue. The present results suggest that the HO-1 pathway is involved in the mediation of delayed cardioprotection by heat stress in rats.

Animals↗

PubMed2002

Involvement of alpha-calcitonin gene-related peptide in heat stress-induced delayed preconditioning in rat hearts.

1. Previous studies have shown that hyperthermia is capable of activating capsaicin-sensitive sensory nerves and stimulating the release of neurotransmitters from their peripheral terminals. Calcitonin gene-related peptide (CGRP) has recently been found to participate in delayed cardioprotection in rat isolated hearts. 2. The purpose of the present study was to explore whether the delayed cardioprotection by heat stress in vivo involves the expression and release of CGRP. 3. Sprague-Dawley rats were pretreated with whole-body hyperthermia (rectal 42 degrees C) for 15 min, 24 h before the experiments and then the left main coronary artery of rat hearts was subjected to a 45 min occlusion followed by 3 h reperfusion. The degree of myocardial injury was evaluated by measurement of infarct size and plasma creatine kinase (CK) activity. The plasma levels of CGRP and expression of CGRP (alpha and beta isoforms) mRNA in lumbar dorsal root ganglia at 4, 8, 16 or 24 h after heat stress treatment were measured. 4. Pretreatment with hyperthermia significantly reduced infarct size and CK release. Heat stress also significantly increased plasma concentrations of CGRP and the expression of alpha-CGRP mRNA, but not beta-CGRP mRNA. The effect of heat stress was completely abolished by pretreatment with capsaicin (50 mg/kg, s.c.), which selectively depletes transmitters in capsaicin-sensitive sensory nerves. 5. In summary, the results suggest that the delayed cardioprotection by heat stress involves the synthesis and release of CGRP and that the protection is mainly mediated by the alpha-CGRP isoform.

Animals↗

PubMed2002

The cardioprotection of rutaecarpine is mediated by endogenous calcitonin related-gene peptide through activation of vanilloid receptors in guinea-pig hearts.

Previous investigations have shown that calcitonin gene-related peptide (CGRP) protects against myocardial ischemia-reperfusion injury and that rutaecarpine activates vanilloid receptors to evoke CGRP release. In the present study, we examined whether rutaecarpine enhances preservation with cardioplegia in guinea-pig hearts, and whether the protective effects of rutaecarpine are related to stimulation of endogenous CGRP release via activating vanilloid receptors. The isolated guinea-pig heart was arrested using St. Thomas Hospital solution, and then reperfused with normothermic Krebs-Henseleit solution for 30 min after a 4-h hypothermic ischemic period. Hypothermic ischemia caused a decline in cardiac function (left ventricular pressure, +/-dp/dt(max), heart rate and coronary flow) and an increased release of creatine kinase during reperfusion. Rutaecarpine at the concentration of 1.0 microM significantly improved the recovery of cardiac function and reduced the release of creatine kinase during reperfusion after hypothermic ischemia. Rutaecarpine at the concentration of 3.0 microM significantly reduced the release of creatine kinase and increased the coronary flow, but only caused a slight improvement of left ventricular pressure, +/-dp/dt(max), heart rate during reperfusion. The cardioprotective effects of rutaecarpine were abolished by capsazepine, a competitive vanilloid receptor antagonist, or by CGRP (8-37), a selective CGRP receptor antagonist. Rutaecarpine at the concentration of 1.0 or 3.0 microM significantly increased the release of CGRP, which was also abolished by capsazepine. These results suggest that rutaecarpine enhances preservation with cardioplegia in guinea-pig hearts and that the protective effects of rutaecarpine are due to stimulation of endogenous CGRP release via activating vanilloid receptors.

Alkaloids↗