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Increasing evidence suggests that transmembrane protein 16A (TMEM16A) in nociceptive neurons is an important molecular component contributing to peripheral pain transduction. The present study aimed to evaluate the role and mechanism of TMEM16A in chronic nociceptive responses elicited by spared nerve injury (SNI). In this study, SNI was used to induce neuropathic pain. Drugs were administered intrathecally. The expression and cellular localization of TMEM16A, the ERK pathway, and NK-1 in the dorsal root ganglion (DRG) were detected by western blot and immunofluorescence. Behavioral tests were used to evaluate the role of TMEM16A and p-ERK in SNI-induced persistent pain and hypersensitivity. The role of TMEM16A in the hyperexcitability of primary nociceptor neurons was assessed by electrophysiological recording. The results show that TMEM16A, p-ERK, and NK-1 are predominantly expressed in small neurons associated with nociceptive sensation. TMEM16A is colocalized with p-ERK/NK-1 in DRG. TMEM16A, the MEK/ERK pathway, and NK-1 are activated in DRG after SNI. ERK inhibitor or TMEM16A antagonist prevents SNI-induced allodynia. ERK and NK-1 are downstream of TMEM16A activation. Electrophysiological recording showed that CaCC current increases and intrathecal application of T16Ainh-A01, a selective TMEM16A inhibitor, reverses the hyperexcitability of DRG neurons harvested from rats after SNI. We conclude that TMEM16A activation in DRG leads to a positive interaction of the ERK pathway with activation of NK-1 production and is involved in the development of neuropathic pain after SNI. Also, the blockade of TMEM16A or inhibition of the downstream ERK pathway or NK-1 upregulation may prevent the development of neuropathic pain. Supplementary Information The online version contains supplementary material available at 10.1007/s12035-021-02520-9.

Pulmonary vascular remodelling is one of the most important factors for pulmonary hypertension (PH). Galectin-3 (Gal-3) is a β-galactoside-binding lectin. In the latest literature, Gal-3 has been reported to be involved in pulmonary vascular remodelling, and its underlying mechanism is unclear. Our research aims to prove the effect of Gal-3 on the proliferation and migration of human pulmonary artery smooth muscle cells (HPASMC) induced by transforming growth factor β1 (TGF-β1) and to study its mechanism. In vivo experiment: In Sprague-Dawley (SD) rats, monocrotaline was injected intraperitoneally to establish a PH model, and the Gal-3 inhibitor (modified citrus pectin, MCP) 28 Ds was administered in the stomach. The results indicate that Gal-3 and TGF-β1 may be involved in the occurrence and development of PH, which may be related to the Smad2/3 signalling pathway. In vitro experiment: Human pulmonary artery smooth muscle cells were pretreated with the Gal-3 inhibitor (MCP) for 24 h, then TGF-β1 or Gal-3 was administered to the cells for 24 h. The results show that exogenous TGF-β1 and Gal-3 can activate the downstream Smad2/3 signalling pathway, and increase the proliferation and migration ability of HPASMC. However, the Gal-3 inhibitor (MCP) inhibited these effects. Further results display that TGF-β1 and Gal-3 could mutually regulate the protein and mRNA expression levels. In summary, the results of this study indicate that Gal-3 regulates the Smad2/3 signalling pathway through protein interaction with TGF-β1, in turn regulates the proliferation and migration of HPASMC, thereby regulating the occurrence and development of PH.

To analyze the effectiveness of Chinese medicine and integrated Chinese and Western medicine for influenza A (H1N1) in the fever clinics and its relevant expenditure.A prospective survey on the clinical epidemic observation and follow-up was conducted from July 2009 to October 2009 with a self-developed questionnaire whose contents including the clinical data of the confirmed 149 H1N1 cases and their relevant therapeutic expenditure. The patients were assigned to the Chinese medicine group (22 cases treated by Chinese medicine alone) and integrative medicine group (124 cases treated by both Chinese medicine and Western medicine). The data were processed with descriptive analysis, t test and χ (2), and sum-rank test.The proportion of clinical recovery of Chinese medicine group (81.8%) was higher than that of integrative medicine group (54.8%) with statistical significance (P=0.02). The average fever durations in both groups were 3.5 to 4 days, showing no significant difference (P=0.86). In the comparisons of average cost of Chinese herbs, drugs, therapies, and total cost, those of the Chinese medicine group were lower than those in the integrative group (P=0.01, P=0.00, P=0.00, P=0.00).The H1N1 patients in the fever clinic who received Chinese medicine treatment had a higher clinical recovery proportion than those who received integrated Chinese and Western medicine treatment with lower medical cost. However, due to small sample size of the Chinese medicine group in the study, the conclusion needs further confirmation by studies with large sample size.