Liver ischemia-reperfusion injury (LIRI) is a pathological process involving multiple injury factors and cell types, with different stages. Currently, protective drugs targeting a single condition are limited in efficacy, and interventions on immune cells will also be accompanied by a series of side effects. In the current bottleneck research stage, the multi-target and obvious clinical efficacy of Chinese medicine (CM) is expected to become a breakthrough point in the research and development of new drugs. In this review, we summarize the roles of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in various stages of hepatic ischemia-reperfusion and on various types of cells. Combined with the current research progress in reducing ROS/RNS with CM, new therapies and mechanisms for the treatment of hepatic ischemia-reperfusion are discussed.
Reperfusion Injury/drug therapy* ; Reactive Oxygen Species/metabolism* ; Reactive Nitrogen Species/metabolism* ; Humans ; Liver/drug effects* ; Animals ; Medicine, Chinese Traditional ; Drugs, Chinese Herbal/pharmacology*

Central nervous system(CNS)degenerative disorders refer to a spectrum of pathological alterations triggered by struc-tural damage to cerebral neural tissues,clinically manifested as diverse neurological dysfunction syndromes,including multiple sclerosis(MS),neurodegenerative diseases(NDs),and ische-mic stroke.The hallmark pathological features of these disorders involve irreversible neuronal damage and decompensation of functional neural networks,ultimately leading to progressive neurological deficits.Notably,with the accelerating global popu-lation aging,the incidence of these diseases has surged signifi-cantly.According to WHO statistics,they now rank among the top three global causes of disability and mortality.Current re-search has confirmed that the pathogenesis of CNS degenerative disorders exhibits high heterogeneity,encompassing multifaceted pathophysiological processes such as genetic predisposition,oxi-dative stress,protein misfolding,and metabolic dysregulation.This intricate pathogenic network not only complicates clinical differential diagnosis but also poses substantial challenges to the development of precision therapeutic strategies.Importantly,re-cent studies have revealed that mitochondrial homeostasis disrup-tion-induced inflammatory cascades(termed mitochondrial in-flammation)play a pivotal regulatory role in neurodegenerative progression.Key molecular mechanisms include impaired mito-phagy,aberrant mitochondrial DNA(mtDNA)release and NL-RP3 inflammasome activation.This review systematically deci-phers the molecular regulatory network of mitochondrial inflam-mation,with a focus on its biological effects in critical pathologi-cal events such as blood-brain barrier disruption,microglial hy-peractivation and neuronal apoptosis.The overarching aim is to provide a theoretical foundation for developing innovative thera-peutic strategies targeting mitochondrial homeostasis restoration.

Central nervous system(CNS)degenerative disorders refer to a spectrum of pathological alterations triggered by struc-tural damage to cerebral neural tissues,clinically manifested as diverse neurological dysfunction syndromes,including multiple sclerosis(MS),neurodegenerative diseases(NDs),and ische-mic stroke.The hallmark pathological features of these disorders involve irreversible neuronal damage and decompensation of functional neural networks,ultimately leading to progressive neurological deficits.Notably,with the accelerating global popu-lation aging,the incidence of these diseases has surged signifi-cantly.According to WHO statistics,they now rank among the top three global causes of disability and mortality.Current re-search has confirmed that the pathogenesis of CNS degenerative disorders exhibits high heterogeneity,encompassing multifaceted pathophysiological processes such as genetic predisposition,oxi-dative stress,protein misfolding,and metabolic dysregulation.This intricate pathogenic network not only complicates clinical differential diagnosis but also poses substantial challenges to the development of precision therapeutic strategies.Importantly,re-cent studies have revealed that mitochondrial homeostasis disrup-tion-induced inflammatory cascades(termed mitochondrial in-flammation)play a pivotal regulatory role in neurodegenerative progression.Key molecular mechanisms include impaired mito-phagy,aberrant mitochondrial DNA(mtDNA)release and NL-RP3 inflammasome activation.This review systematically deci-phers the molecular regulatory network of mitochondrial inflam-mation,with a focus on its biological effects in critical pathologi-cal events such as blood-brain barrier disruption,microglial hy-peractivation and neuronal apoptosis.The overarching aim is to provide a theoretical foundation for developing innovative thera-peutic strategies targeting mitochondrial homeostasis restoration.

Tibetan medicine is an essential part of Chinese medicine and has unique theoretical experience and therapeutic advantages. According to the development principle of inheriting the essence, sticking to the truth, and keeping innovative, the supervision department should give clear and reasonable guidance considering the characteristics of Tibetan medicine, establish a standard system for quality control, clinical verification and evaluation, and accelerate the research and commercialization of new drugs. In view of the needs of drug supply-side reform and the current situation of Tibetan medicine and new pharmaceutical research, we ponder and provide suggestions on the confusion faced by the current supervision of Tibetan drug registration, hoping to contribute to the supervision strategy of Tibetan drug registration and the high-quality development of Tibetan medicine industry.
Tibet ; Medicine, Tibetan Traditional ; Quality Control ; Pharmaceutical Research ; Drug Industry

Aim To investigate the effeet of Eehinaeo- side ( ECH ) regulating the expression of prohibitin (PHB) on MPP+ -induced apoptosis of SH-SY5Y eells and the underlying mechanism.Methods SH-SY5Y eells were seleeted and divided into control group, MPP+ group, MPP+ + ECH group, NC + MPP + group, NC + MPP+ + ECH group, PHB-RNAi + MPP + + ECH group.Cell survival rate was determined by CCK-8 assay.Cell morphology was observed using an inverted phase contrast mieroscope; the apoptotie eells were observed by Hoechst33342 fluorescence staining, whereas apoptotie rate, reactive oxygen speeies eon- tent, and mitochondrial membrane potential were ana¬lyzed by flow eytometry.The relative protein expres¬sions of PHB, Akt, p-Akt, Bel-2, Bax, and cleaved- easpase3 were determined by Western blot.Results Compared with eontrol group, the eell survival rate of MPP+ group signifieantly deereased.The growth state of the eells beeame significantly worse.Intracellular ROS content inereased, mitoehondrial membrane po tential decreased, apoptosis-related protein expression increased and the apoptotic rate increased.Compared with MPP+ group, MPP+ + ECH group significantly increased cell viability.The growth status of cells was significantly improved.Intracellular ROS content de¬creased, mitochondrial membrane potential increased, apoptosis-related protein expression decreased, and the apoptotic rate decreased significantly.The expression levels of PHB and p-Akt significantly increased.Com¬pared with NC + MPP+ + ECH group, p-Akt level de¬creased and the cell apoptotic rate increased in PHB- RNAi +MPP+ + ECH group.Conclusions Echino- side can reduce MPP + - induced apoptosis of SH-SY5Y cells, which may be realized by upregulating PHB ex¬pression and phosphorylation of Akt to protect mito¬chondrial function.

OBJECTIVE: To observe the effect of transcutaneous electrical acupoint stimulation (TEAS) on venous thrombosis and quality of life after lung cancer surgery, basing on the conventional nursing and early functional exercise. METHODS: A total of 120 patients diagnosed as non-small cell lung cancer (NSCLC) and received radical resection of lung cancer surgery for the first time were randomized into a conventional nursing group, a rehabilitation training group and a TEAS group, 40 cases in each group. Conventional nursing was adopted in the conventional nursing group. Conventional nursing combined with early functional exercise were adopted in the rehabilitation training group, the exercise was taken 20 min each time, once in both morning and afternoon for 5 days. On the basis of the treatment in the rehabilitation training group, TEAS was applied at Zusanli (ST 36), Xuehai (SP 10), Sanyinjiao (SP 6), etc. in the TEAS group, with disperse-dense wave in frequency of 30 Hz/100 Hz and tolerable intensity, 30 min each time, once in both morning and afternoon for 5 days. The incidence of venous thrombosis in each group was observed at the 5th day after surgery. Before surgery and at the 5th day after surgery, the Caprini thrombus risk assessment was performed, the Karnofsky performance status (KPS) scale and the functional assessment of cancer therapy-lung (FACT-L) were used to evaluate the quality of life. RESULTS: At the 5th day after surgery, no thrombosis was found in the TEAS group, the incidence of venous thrombosis in the TEAS group was lower than 15.0% (6/40) in the conventional nursing group ( CONCLUSION On the basis of the conventional nursing and early functional exercise, TEAS can reduce the incidence of venous thrombosis, effectively prevent thrombosis and improve quality of life.
Acupuncture Points ; Carcinoma, Non-Small-Cell Lung/surgery* ; Humans ; Lung Neoplasms/surgery* ; Quality of Life ; Transcutaneous Electric Nerve Stimulation ; Venous Thrombosis/etiology*

Polysaccharide from traditional Chinese herb, Saposhnikovia divaricata (Turcz.) Schischk. (SD) was extracted, fractionated and characterized in this work. Four fractions were prepared. Their molecular weight, monosaccharide compositions, linkage modes and structural properties were characterized with SEC-MALS-RI, HPAEC-PAD, GC-MS and NMR. SDP1 was assigned as a 1, 4-α-glucan with small amount of O-6 linked branches. SDP2 contained a big amount of the 1, 4-α-glucan and a small amount of arabinogalactan, while SDP3 possessed relatively lower amount of the 1, 4-α-glucan and a big amount of the arabinogalactan. SDP4 was defined as a pectic arabinogalactan. Four fractions showed antioxidant activities in both molecular and cellular levels and their activity was ranked as SDP4 ≈ SDP3>SDP2>SDP1. The 1, 4-α-glucan in SDP1 had the weakest, while SDP3 and SDP4 showed similar and the highest antioxidant activity. The arabinogalactan was the major component of both SDP3 and SDP4, which significantly contributed to the antioxidant activity of SDP.

BackgroundFacioscapulohumeral muscular dystrophy (FSHD) is characterized by asymmetric muscular deficit of facial, shoulder-girdle muscles, and descending to lower limb muscles, but it exists in several extramuscular manifestations or overlapping syndromes. Herein, we report a "complex disease plus" patient with FSHD1, accompanied by peripheral neuropathy and myoclonic epilepsy.

MethodsStandard clinical assessments, particular auxiliary examination, histological analysis, and molecular analysis were performed through the new Comprehensive Clinical Evaluation Form, pulsed-field gel electrophoresis-based Southern blot, Multiplex Ligation-dependent Probe Amplification (MLPA), whole exome sequencing (WES), and targeted methylation sequencing.

ResultsThe patient presented with mild facial weakness, humeral poly-hill sign, scapular winging, peroneal weakness, drop foot, pes cavus, and myoclonic epilepsy. Furthermore, electrophysiology revealed severely demyelinated and axonal injury. The muscle and nerve biopsy revealed broadly fiber Type II grouping atrophy and myelinated nerve fibers that significantly decreased with thin myelinated fibers and onion bulbs changes. Generalized sharp and sharp-slow wave complexes on electroencephalography support the diagnosis toward myoclonic epilepsy. In addition, molecular testing demonstrated a co-segregated 20-kb 4q35-EcoRI fragment and permissive allele A, which corresponded with D4Z4 hypomethylation status in the family. Both the patient's mother and brother only presented the typical FSHD but lacked overlapping syndromes. However, no mutations for hereditary peripheral neuropathy and myoclonic epilepsy were discovered by MLPA and WES.

ConclusionsThe present study described a "tripe trouble" with FSHD, peripheral neuropathy, and myoclonic epilepsy, adding the spectrum of overlapping syndromes and contributing to the credible diagnosis of atypical phenotype. It would provide a direct clue on medical care and genetic counseling.

Adult ; Child ; Epilepsies, Myoclonic ; complications ; Evoked Potentials, Visual ; Humans ; Male ; Muscle, Skeletal ; Muscular Dystrophy, Facioscapulohumeral ; complications ; Peripheral Nervous System Diseases ; complications

Objective To investigate the protective effect and mechanism of environmental enrichment(EE)on radiation induced cognitive dysfunction in mice.Methods A total of 45 female Kunming mice(2-month old)were randomly divided into control group,irradiation group and irradiation plus EE group with 15 in each group.Irradiation group and irradiation plus EE group were treated with a single dose of 4 Gy whole body irradiation,irradiation plus EE group were housed in EE condition for 35 d after irradiation.The object recognition task was used to evaluate the cognitive function of mice.The expression of microglial marker IBA-1 in hippocampus was determined by immunohistochemical staining.The expressions of CD68 and synaptophysin(SYP)proteins in hippocampus were assayed by Western blot.Results Compared with control group,the irradiation group had a low discrimination ratio in object recognition task and had a remarkable low level of SYP expression in hippocampus(t＝3.66,6.84,P＜0.05).In addition,radiation activated microglia in hippocampus by increasing the number of IBA-1-positive cells and enhancing the expression of CD 68(t ＝6.83,5.79,P ＜0.05).Compared with irradiation group,irradiation plus EE group increased the discrimination ratio and the expression of SYP in hippocampus(t＝3.56,4.06,P＜0.05),while the number of IBA-1-positive cells and the expression of CD68 were significantly reduced(t＝7.69,4.59,P＜0.05).Conclusions A single dose of 4 Gy whole body irradiation leads to cognitive dysfunction in mice,while EE could effectively improve the animals′cognitive behavior possibly by inhibiting microglial activation and preventing synapse loss in hippocampus.

OBJECTIVETo explore the coexistence of ASXL1 and CALR gene mutations in patients with essential thrombocytheima (ET) and with primary myelofibrosis(PMF), and to compare the differences of clinical characteristics between ET and PMF patients carrying ASXL1 and CALR mutations, and ET and PMF patients carrying solitary gene mutation, and ET and PMF patients without any mutations.

METHODSThe mutations of ASXL1 gene at exon 12, CALR gene at exon 9 and MPL gene at exon 10 in 263 essential ET patients and 29 PMF patients were detected by PCR amplification followed by direct sequencing of genomic DNA. The JAK2V617F mutations were used by allele specific PCR detection.

RESULTS72.6%(212/292)of patients harbored at least one mutation. The incidences of ASXL1 and CALR mutations were 5.8% and 30.5%, respectively. The frequencies of JAK2V617F and MPL mutations were 39.0% and 2.4%, respectively. 5.1%(15/292) of patients had double mutations, including ASXL1 and CALR(n=11), ASXL1 and JAK2V617F(n=2), MPL and CALR(n=1) and ASXL1 and MPL(n=1). The frequency of concurrent ASXL1 and CALR mutations was found to be high. Significant difference was found on hemoglobin levels and platelet counts between CALR and ASXL1 mutations and single mutation (P<0.05),however, the difference on leukocyte counts and median age was not found. Compared with negative patients, the presence of ASXL1 and CALR mutations was found to be significantly correlative with lower hemoglobin level (P=0.045), lower leukocyte count (P=0.002) and with higher platelet counts(P=0.001), but the difference of median age was not found.

CONCLUSIONThe frequency of concurrent ASXL1 and CALR mutations is higher in ET patients. The coexistence of ASXL1 and CALR gene mutations significantly associated with lower hemoglobin level and higher platelet count.