ABSTRACT
Ficus hirta Vahl. is a Moraceae plant, named for its palm-like leaves. It is a widely used traditional medicinal material with definite curative effect. At the same time, it is also a commonly used soup material among the folk in South China. In March 2022, a serious leaf spot disease with symptoms similar to anthracnose was observed on F. hirta in several plantations in Qinzhou and Zhanjiang City of China, with an incidence of 32~65%. The early symptoms of infected leaves were small, round, yellow spots that further expanded into larger, brown, irregular, necrotic lesions surrounded by dark brown edges, which eventually led to leaf wilt. Twenty symptomatic leaves were collected from three plantations with a total area of about 10 hm2. Fragments (2×2 mm) from the 20 infected leaves were surface sterilized, plated on potato dextrose agar (PDA) and incubated at 28°C. After 3 days, isolates with similar cultural morphology were obtained and three representative isolates (WZMT-1, WZMT-3 and WZMT-8) were randomly selected for following study. The colonies by single-spore purification on PDA were initially cottony, pale white and became grayish green with age. The conidia were hyaline, abundant, cylindrical, with rounded ends, 14.4~18.2 µm×4.6~6.0 µm (av. 16.2 µm×5.4 µm, n=100). Conidiogenous cells hyaline, cylindrical or ampulliform, 6.2~22.7 µm × 2.7~5.0 µm (av. 12.9 µm×3.8 µm, n=50). Appressoria were brown to dark brown, ovoid to clavate, elliptical or irregular, 7.9~13.4 µm × 5.6~9.2 µm (av. 10.6 µm×7.9 µm, n=50). The morphology of the fungus resembled Colletotrichum fructicola (Prihastuti et al. 2009). For molecular identification, the internal transcribed spacer (ITS) regions, glyceraldehyde-3-phosphatedehydrogenase (GAPDH), actin (ACT), beta-tubulin 2 (TUB2), calmodulin (CAL), partial manganese superoxide dismutase (sod2), partial Apn2-Mat1-2 intergenic spacer and partial mating type (Mat1-2) (ApMat) genes were amplified from genomic DNA for the isolates using the primers described by Silva et al. (2012) and Weir et al. (2012). The sequences of the above seven loci of the three isolates (accession nos. OQ121661 to OQ121663 and OQ133400 to OQ133417) were obtained and showed over 99% identity with the existing sequences of ex-type culture ICMP 18581 of Colletotrichum fructicola (Weir et al. 2012). A multilocus phylogenetic analysis of the seven loci concatenated sequences using the maximum likelihood method revealed that the isolates belong to C. fructicola. To confirm pathogenicity, five 3-month-old potted plants were used for inoculation with each representative isolate. Tested plants were sprayed with 10 ml of a conidial suspension (1 × 108 conidia/ml) , and the controls plants were sprayed with sterile water. All the plants were incubated in a growth chamber at 26 ± 2°C with 95% relative humidity. After 10 days, typical lesions like those observed on the field plants appeared on all inoculated plants, while the control remained healthy. The same fungal pathogen was reisolated and the identity was confirmed by morphological characterization and molecular analysis, confirming Koch's postulates. The pathogen has been reported as the causal agent of anthracnose on a wide range of plant hosts worldwide (Marquez-Zequera et al. 2018; Horfer et al. 2021; Jiang et al. 2022; Li et al. 2023). To our knowledge, this is the first report of anthracnose on F. hirta caused by C. fructicola in southern China.
ABSTRACT
Myocardial ischemia-reperfusion injury(MIRI) is an urgent problem in clinical treatment. As cardiomyocytes are terminal cells, MIRI-induced cardiomyocyte death will irreversibly damage the structure and function of the heart. In previous studies, apoptosis was considered to be the only way to regulate cell death, while necrosis could not be regulated. However, current studies have shown that cell necrosis could also be regulated, which was collectively called programmed cell death(PCD). Regulated cell death is actively mediated through molecular pathways, so there is the possibility of inhibiting this signaling to reduce MIRI. At present, PCD mainly includes apoptosis, autophagy, necrosis, pyroptosis and ferroptosis. As a unique treature in China, traditional Chinese medicine has the advantages of multiple pathways, multiple targets, low toxicity, less side effects and low economic costs. With the in-depth study of the efficacy of traditional Chinese medicine against MIRI, it has been confirmed that traditional Chinese medicine could regulate PCD to reduce MIRI. Therefore, this paper focuses on the relationship between PCD and MIRI, and new studies on intervention with relevant traditional Chinese medicine, with the aim to provide new MIRI prevention and treatment methods from the perspective of "intervention of PCD".
Subject(s)
Humans , Apoptosis , China , Medicine, Chinese Traditional , Myocardial Reperfusion Injury/genetics , Myocytes, CardiacABSTRACT
Myocardial ischemia-reperfusion injury （MIRI） was originated from the ischemic injury to myocardial cells due to some factors， and the injury will be aggravated after the blood supply recovery. MIRI will cause reperfusion arrhythmia， myocardial stagnation， microcirculation disorders or blood loss reflow， and become a key issue to be solved in the clinical treatment. Therefore， it is of important clinical significance to explore how to improve MIRI. The phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway has been regarded to be an important cascade signaling pathway to prevent MIRI， which is cross-talked in such mechanisms as oxidative stress， calcium overload， autophagy， inflammation， endoplasmic reticulum stress and mitochondrial dysfunction. This pathway is at the core site and closely related to the severity of MIRI. Meanwhile， traditional Chinese medicine（TCM） has its unique advantages in the prevention and treatment of MIRI， including multiple targets， multiple pathways， fewer toxic and side effect， as well as TCM characteristics of syndrome differentiation treatment and overall concept. A great number of studies have confirmed that this pathway is a common mechanism of action for most TCM compounds， TCM monomers and extracts. In this paper， we clarify the effect of PI3K/Akt signaling pathway crosstalk on the myocardial ischemia-reperfusion injury， with the focus on the relationship between the key targets of PI3K/Akt signaling pathway and MIRI. It will give great insights to the intricate relationship between them and promote the future development of new drugs targeting the PI3K/Akt signaling pathway. Finally， we also summarized the existing findings of TCM on PI3K/Akt pathway， which provides a reference for the treatment and drug development of MIRI.
ABSTRACT
<p><b>OBJECTIVE</b>To observe the morphological changes in enteric nerve system (ENS) of rats with multiple organ dysfunction syndrome (MODS) treated by Dachengqi Decoction (, DCQD).</p><p><b>METHODS</b>Fifty Wistar rats were randomly assigned to the control group, MODS model group and DCQD treated group. The rats in MODS model group and DCQD treated group were injected Escherichia coli (E. coli) suspension into abdominal cavity under sterile condition. The DCQD treated group was gavaged with DCQD 2 days before the E. coli suspension was injected. Twenty-four hours after injection, the proximal segment of intestine was resected and studied by immunohistofluorescence using vesicular acetylcholine transporter, vasoactive intestinal polypeptide (VIP), substance P (SP) and neuronal nitric oxide synthase (nNOS) antibodies. The whole-mount preparations were observed by laser scanning confocal microscope to detect the changes of quantity and fluorescence integral optical density (IOD) value of intestine enteric nerves.</p><p><b>RESULTS</b>Compared with the control group, the quantity and IOD value of acetylcholine (ACh), VIP, SP and nitric oxide (NO) nerves of intestine in the MODS group were significantly decreased (P<0.01), and the network of enteric nerves was remarkably disrupted. Compared with the MODS group, the quantity and fluorescence IOD value of ACh, VIP, SP and NO nerves in the DCQD group were significantly increased (P<0.01), and the network of enteric nerves was remarkably recovered.</p><p><b>CONCLUSION</b>DCQD can protect and repair damage in the network of ACh, SP, NO and VIP nerves in rats with MODS, which may be one of mechanisms involved in promoting gastrointestinal motility by DCQD.</p>
Subject(s)
Animals , Female , Male , Rats , Enteric Nervous System , Pathology , Multiple Organ Failure , Pathology , Plant Extracts , Pharmacology , Rats, WistarABSTRACT
<p><b>OBJECTIVE</b>To observe the intervention of Dachengqi Granule (DG) on the apoptosis of small intestine smooth muscle cells (SMCs) in rats with multiple organ dysfunction syndrome (MODS) and its mechanisms.</p><p><b>METHODS</b>Healthy 100 adult Wistar rats were randomly divided into the control group (n =20), the MODS model group (n =40), and the DG group (n =40).E. coli suspension was peritoneally injected to rats in the model group and the DG group to establish bacterial peritonitis induced MODS model. DG at 1 mL/100 g was administered by gastrogavage to rats of the DG group, twice daily for 3 successive days. Twenty-four hours after modeling, the proximal segment of intestine was taken and stained by using terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) and immunohistochemistry. Changes of apoptosis quantity of SMCs and the expression of Bcl-2 associated X protein (Bax), B cell lymphoma/leukemia-2 (Bcl-2) and cytochrome c protein (Cyt c) in mitochondrial apoptotic signaling pathway were observed.</p><p><b>RESULTS</b>Compared with the control group, the apoptosis quantity of SMCs and the expression of Bax and Cyt c protein significantly increased, and the expression of Bcl-2 protein significantly decreased in the MODS model group (P <0.01). Compared with the MODS model group, the apoptosis quantity of SMCs and the expression of Bax and Cyt c proteins significantly decreased, and the expression of Bcl-2 protein significantly increased in the DG group (allP <0.01).</p><p><b>CONCLUSION</b>DG could inhibit apoptosis of SMCs through suppressing activation of mitochondrial apoptotic signaling pathway in intestinal SMCs, thus promoting the recovery of the gastrointestinal motility function in rats with MODS.</p>