Comparative Analysis of Acanthopanacis Cortex and Periplocae Cortex Using an Electronic Nose and Gas Chromatography-Mass Spectrometry Coupled with Multivariate Statistical Analysis.

Chinese Herbal Medicines (CHMs) can be identified by experts according to their odors. However, the identification of these medicines is subjective and requires long-term experience. The samples of Acanthopanacis Cortex and Periplocae Cortex used were dried cortexes, which are often confused in the market due to their similar appearance, but their chemical composition and odor are different. The clinical use of the two herbs is different, but the phenomenon of being confused with each other often occurs. Therefore, we used an electronic nose (E-nose) to explore the differences in odor information between the two species for fast and robust discrimination, in order to provide a scientific basis for avoiding confusion and misuse in the process of production, circulation and clinical use. In this study, the odor and volatile components of these two medicinal materials were detected by the E-nose and by gas chromatography-mass spectrometry (GC-MS), respectively. An E-nose combined with pattern analysis methods such as principal component analysis (PCA) and partial least squares (PLS) was used to discriminate the cortex samples. The E-nose was used to determine the odors of the samples and enable rapid differentiation of Acanthopanacis Cortex and Periplocae Cortex. GC-MS was utilized to reveal the differences between the volatile constituents of Acanthopanacis Cortex and Periplocae Cortex. In all, 82 components including 9 co-contained components were extracted by chromatographic peak integration and matching, and 24 constituents could be used as chemical markers to distinguish these two species. The E-nose detection technology is able to discriminate between Acanthopanacis Cortex and Periplocae Cortex, with GC-MS providing support to determine the material basis of the E-nose sensors' response. The proposed method is rapid, simple, eco-friendly and can successfully differentiate these two medicinal materials by their odors. It can be applied to quality control links such as online detection, and also provide reference for the establishment of other rapid detection methods. The further development and utilization of this technology is conducive to the further supervision of the quality of CHMs and the healthy development of the industry.

CCL2-CCR2 Axis Potentiates NMDA Receptor Signaling to Aggravate Neuropathic Pain Induced by Brachial Plexus Avulsion.

Brachial plexus avulsion (BPA) represents the most devastating nerve injury in the upper extremity and is always considered as a sophisticated problem due to its resistance to most standard pain relief medications or neurosurgical interventions. There is also a lack of understanding on the underlying mechanisms. Our study aimed to investigate whether spinal CCL2-CCR2 signaling contributed to the development of neuropathic pain following BPA via modulating glutamate N-methyl-d-aspartate receptor (NMDAR). A rat model of BPA on lower trunk (C8-T1) was established, and the sham- and BPA-operated animals were intrathecally injected with saline, C-C chemokine receptor type 2 (CCR2) inhibitor INCB3344 and NMDAR antagonist DL-AP5 one week postoperatively, the behavioral performance of the treated animals and expressions of C-C motif ligand 2 (CCL2), CCR2, and N-methyl-D-aspartic acid receptor 2B (NR2B) in spinal cord sections of each group were examined. It was shown that BPA injury significantly reduced mechanic withdrawal thresholds the next day after surgery until the end of the observation. Both CCL2 and CCR2 expressions increased in BPA rats compared to those in sham rats. CCL2 was mainly localized in astrocytes, and CCR2 was preferably expressed on astrocytes and neurons. Besides, NMDAR subunit NR2B increased in BPA-operated rats, which was reversed in response to CCR2 and NR2B inhibition. However, these inhibitors didn't change the spinal NMDAR level in sham rats. CCR2 and NMDAR inhibition efficiently alleviated mechanical allodynia caused by BPA either at early or late phase of neuropathic pain. Collectively, CCL2-CCR2 axis is associated with mechanical pain after BPA by elevating NMDAR signaling.

[The timing of infusion of hypertonic saline to exert protective effect on intestinal barrier function in the rabbit with intestinal ischemia/reperfusion injury].

OBJECTIVE: To study the timing of infusion of hypertonic saline solution (HTS) to exert its protective effect on intestinal barrier function in rabbits with intestinal ischemia/reperfusion (I/R) injury. METHODS: Seventy-two rabbits were randomly divided into four groups (each n=18): sham operation group, I/R group, HTS pretreatment group and HTS delayed treatment group. The intestinal I/R models were produced by blocking the superior mesenteric artery (SMA) for 1 hour followed by release of the SMA. 7.5% HTS (6 ml/kg) was infused in HTS pretreatment group 5 minutes before release of SMA, and HTS was infused in delayed treatment group 2 hours after reperfusion and finished in 5 minutes. Levels of D-lactic acid (D-Lac), lipopolysaccharide (LPS), tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10) were determined before ischemia and 2, 4, 6 hours after reperfusion. The levels of malonaldehyde (MDA), superoxide dismutase (SOD), myeloperoxidase (MPO) in intestinal tissues of 8 rabbits in each group were measured at 6 hours after reperfusion. Meanwhile the intestinal morphological changes were observed, and the Chin score, which reflected the degree of injury to intestinal mucosa was calculated. RESULTS: Compared with sham operation group, D-Lac, LPS, TNF-α and IL-10 in I/R group were significantly increased from 2 hours after reperfusion (D-Lac: 18.91 ± 3.46 mg/L vs. 3.92 ± 0.61 mg/L, LPS: 869 ± 85 EU/L vs. 422 ± 27 EU/L, TNF-α: 23.80 ± 4.22 µg/L vs. 3.65 ± 0.51µg/L, IL-10: 8.90 ± 2.75 µg/L vs. 2.53 ± 0.80 µg/L, all P<0.05); MDA, MPO and Chiu score were significantly increased (MDA: 398 ± 28 nmol/mg vs. 173 ± 20 nmol/mg, MPO: 465 ± 52 mU/mg vs. 183 ± 25 mU/mg, Chiu score: 4.36 ± 0.52 vs. 0.38 ± 0.22, all P<0.05), while SOD decreased significantly (35 ± 9 U/mg vs. 52 ± 8 U/mg, P<0.05). Compared with I/R group, the levels of D-Lac, LPS, TNF-α, MDA, MPO and Chiu score in HTS pretreatment group were lower (D-Lac: 11.45 ± 0.92 mg/L vs. 18.91 ± 3.46 mg/L, LPS: 455 ± 114 EU/L vs. 869 ± 85 EU/L, TNF-α: 10.32 ± 2.11 µg/L vs. 23.80 ± 4.22 µg/L, MDA: 221 ± 21 nmol/mg vs. 398 ± 28 nmol/mg, MPO: 271 ± 20 mU/mg vs. 465 ± 52 mU/mg, Chiu score: 1.69 ± 0.24 vs. 4.36 ± 0.52, all P<0.05), while IL-10 and SOD were significantly increased (IL-10: 14.54 ± 2.02 µg/L vs. 8.90 ± 2.75 µg/L, SOD: 90 ± 14 U/mg vs. 35 ± 9 U/mg, both P<0.05). The levels of the above indexes in HTS delayed treatment group were similar to I/R group, and the effect was lower than that in HTS pretreatment group. CONCLUSIONS: HTS had the protective effect on intestine suffering from I/R injury. But the protective effect was time dependent, and early treatment shows protective effect.

[Apoptosis of gastric mucosa and gastric barrier dysfunction in acute ischemic stroke].

OBJECTIVE: To evaluate the role of gastric mucosa apoptosis in the stress of ischemic stroke, and to discuss the relationship between gastric mucosa apoptosis and gastric barrier. METHODS: Ten dogs were artificially made ischemic stroke by operation (IS group), and another 10 shamly-operated dogs were served as control group. Sucrose permeability were measured after the operation. All dogs were sacrificed 24 hours after operation to measure the gastric mucosal apoptosis index, gastric gross classification, and histological score. RESULTS: The gastric mucosal apoptosis index in the IS group were significantly higher than in the control group (14.83 +/- 4.41 vs. 5.60 +/- 2.61, P < 0.05). The gastric mucosal apoptosis index were correlated with the sucrose permeability (r = 0. 89, P < 0.05) , gastric gross classification (r = 0. 87, P < 0.05), and histological score (r = 0.92, P < 0.05). CONCLUSIONS: Although ischemic stroke will not cause the obvious damage in the respiratory and circulatory system, it is responsible for the apoptosis of epithelial cell in the gastric mucosa and gastric barrier dysfunction. The apoptosis index is closely correlated with the damage of the function and morphology of the gastric barrier, indicating that the epithelial cell apoptosis acceleration in the gastric mucosa may result in the damage of gastric barrier function.