Ischemic stroke (IS) is a severe cerebrovascular disease with a high incidence, mortality, and disability rate. The first-line treatment for IS is the use of recombinant tissue plasminogen activator (r-tPA). Regrettably, numerous patients encounter delays in treatment due to the narrow therapeutic window and the associated risk of hemorrhage. Traditional Chinese medicine (TCM) has exhibited distinct advantages in preventing and treating IS. TCM enhances cerebral microcirculation, alleviates neurological disorders, regulates energy metabolism, mitigates inflammation, reduces oxidative stress injuries, and inhibits apoptosis, thereby mitigating brain damage and preventing IS recurrence. This article summarizes the etiology, pathogenesis, therapeutic strategies, and relationship with modern biology of IS from the perspective of TCM, describes the advantages of TCM in the treatment of IS, and further reviews the pharmacodynamic characteristics and advantages of TCM in the acute and recovery phases of IS as well as in post-stroke complications. Additionally, it offers valuable insights and references for the clinical application of TCM in IS prevention and treatment, as well as for the development of novel drugs.

Modern medicine has made remarkable achievements in safeguarding people's life and health, however, it is increasingly found that in the face of complex diseases, selective targeting of single target is often difficult to produce a comprehensive rehabilitation effect, and is prone to induce drug resistance, toxic side effects. Traditional Chinese medicine (TCM) has a long history of clinical application, and its clinical value in the treatment of complex diseases such as cardiovascular and cerebrovascular diseases, digestive diseases, skin diseases, rheumatism and immunity diseases, and adjuvant treatment of tumors has been proven to have obvious advantages. However, its modern research is relatively lagging behind, and in the face of the aging society and the characteristics of the modern disease spectrum, the traditional knowledge-driven research paradigm seems to be stuck in a bottleneck and difficult to make greater breakthroughs. Focusing on the key issues of TCM development in the new era, the clinical value-oriented strategy becomes to be a new research paradigm of TCM inheritance and innovation development, and dominant diseases would be the focus of the TCM inheritance and innovation development, which has been highly valued in recent years by the TCM academia and the relevant national management departments. Based on the clinical value, a series of policies are formulated for the selection and evaluation of the TCM dominant diseases (TCMDD), and exploratory researches about the clinical efficacy characteristics, the modern scientific connotation interpretation were carried out. The clinical value-oriented research paradigm of TCMDD inheritance and innovation development has been initially formed, which is characterized by strong policy support as the guarantee, systematic and standardized selection and evaluation methods as the driving force, scientific and effective research on internal mechanisms as the expansion, and effective clinical guidelines and principles as the transformation, which is of great value in promoting the high-quality development of the industries and undertaking of TCM. In this paper, the main policy support, selection and evaluation methods, therapeutic effect characterization, and modern scientific connotation research strategies of TCMDD in recent years have been comprehensively sorted out, with a view to providing the healthy and benign development of the research on TCMDD.

Objective:To investigate the protective effect of carbon monoxide releasing molecule 2 (CORM-2) on intestinal barrier by regulating the differentiation of T lymphocytes in rats with hemorrhagic shock.Methods:Healthy male Sprague-Dawley rats ( n=56) were randomly (random number) divided into the sham operation group, shock group, dimethyl sulfoxide (DMSO) control group, inactivated carbon monoxide release molecule-2 (iCORM-2) pretreatment group and three pretreatment CORM-2 with the doses of 2, 4 and 6 mg/kg separately. The hemorrhagic shock was induced with the use of a modified Wiggers model. Rats in the CORM-2 group and iCORM-2 group were intraperitoneally injected with CORM-2 with the doses of 2, 4 and 6 mg/kg and 6 mg/kg iCORM-2 instantly before shock induction. Rats in the DMSO group received intraperitoneal administration of 2% DMSO with the same volume of iCORM-2. Rats in the shock group and sham operation group were not pretreated before inducing shock. Mean arterial pressure of each rat was recorded at different phases after catheterization or shock. Twenty-three hours after shock induction, the permeability of intestinal barrier was measured by FITC-dextran flux, and then ileum tissues were harvested to observe histopathologic changes. Immunohistochemistry was used to detect the expression of transcription factors T-bet and Foxp3 of intestinal mucosa in rats, and the expression of interferon-γ (IFN-γ), interleukin-10 (IL-10) and transforming growth factor-β (TGF-β) in intestinal mucosa was measured by Western blot. One-way analysis of variance or Kruskal Wallis rank sum test was used to compare the difference among groups for normal or non-normal distributed data. Results:Compared with the sham operation group, serum concentrations of FITC-dextran were significantly increased in the shock group, DMSO group and iCORM-2 group (all P<0.05). The concentrations of FITC-dextran in serum of three CORM-2 pretreatment groups pretreatment were significantly decreased compared with other groups undergoing shock (all P<0.05). Rats in the shock group, DMSO group and iCORM-2 group showed severe ileum injury. CORM-2 intervention resulted in alleviation of intestinal mucosal injury in rats with shock, and rats in groups pretreatment CORM-2 at the doses of 4 and 6 mg/kg exhibited integrity of anatomic ileac structure. Compared with the sham operation group, T-bet levels of intestinal intraepithelial lymphocytes were increased in shock group and DMSO group (all P<0.05). Compared with the shock group, levels of T-bet were decreased in intestinal epithelium of three groups pretreatment with CORM-2 at the doses of 2, 4 and 6 mg/kg (all P<0.05). Foxp3 levels in intestinal intraepithelial lymphocytes of the iCORM-2 group and two groups pretreatment with CORM-2 at the doses of 4 and 6 mg/kg were increased compared with the shock group and DMSO group (all P<0.05), but there was no significant difference among the shock group, DMSO group and group pretreatment with CORM-2 at 6 mg/kg (all P>0.05). The shock group showed increased expression of IFN-γ (all P<0.05), but unchangeable expression of IL-10 and TGF-β (all P>0.05) compared with the sham operation group. Compared with the shock group, the expression levels of IL-10 in three groups pretreatment with CORM-2 at the doses of 2, 4 and 6 mg/kg were significantly increased (all P<0.05), and the expression levels of TGF-β were increased in two groups pretreatment with CORM-2 at the doses of 4 and 6 mg/kg (all P<0.05). The expression of IFN-γ in group pretreatment with CORM-2 at 6 mg/kg was significantly decreased compared with the shock group ( P<0.05). Conclusions:CORM-2 inhibited the activation of type 1 helper T cells to decrease the expression of proinflammatory factors and upregulated the expression of anti-inflammatory factors. Thus, CORM-2 reduced gut inflammation and protected the intestinal barrier.