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Mechanism of action of Linggui Zhugan Decoction in treating non-alcoholic fatty liver disease using untargeted metabolomics approach

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Traditional Medicine Research 2025年第2期10卷 65-76页

作者： Huan Pei Ren-Lin Li Xin-Ran Song Qian-Qian Wan Yu-Ming Wang Han-Zhou Li Wei-Quan Xu Jia-Bao Liao Wei-Bo Wen Jing Miao Huan-Tian Cui School of Basic Medicine Yunnan University of Chinese MedicineKunming 650599China School Clinical medical College Yunnan University of Chinese MedicineKunming 650599China first School of Clinical Medicine Yunnan University of Chinese MedicineKunming 650599China School of Integrative Chinese and Western Medicine Tianjin University of Traditional Chinese MedicineTianjin 301617China Department of Pharmacy Tianjin Second People's HospitalTianjin 300192China

Background:Non-alcoholic fatty liver disease(NAFLD)is a liver disorder characterized by the accumulation and degeneration of fat in the liver cells,a condition that may further deteriorate and lead to cirrhosis and liver *** studies showed that metabolic dysfunction can promote NAFLD *** Zhugan Decoction(LGZGD)has therapeutic effects on *** mechanism of LGZGD still remains *** study was to examine the impact of LGZGD on the metabolic processes involved in the development of ***:A mice model of NAFLD was treated with *** therapeutic potential of LGZGD was evaluated by assessing the activity of transaminases,lipids levels of blood,and pathological changes in the liver of the mice model of ***,this study also evaluated the influence of LGZGD on liver inflammation and oxidative ***:The results of untargeted metabolomics analysis showed that LGZGD reduced the disordered lipid metabolism in NAFLD *** improved the oxidative stress and also reduced the levels of pro-inflammatory cytokines in the *** metabolomics analysis of liver samples revealed that LGZGD treatment improved metabolic disorders,including alanine,aspartate,glutamate,glycerophospholipid metabolism,and citrate *** RT-qPCR and Western blot results showed that LGZGD could regulate the expression of key enzymes in the metabolic pathway of the citrate cycle,including ATP-citrate lyase(ACLY),alanine-glyoxylate aminotransferase-2(AGXT2),phosphatidylethanolamine N-methyltransferase(PEMT),and succinate dehydrogenase(SDH).Conclusion:We found that LGZGD can treat NAFLD by reducing inflammatory responses,inhibiting oxidative stress,regulating alanine,aspartate,glutamate,and glycerophospholipid metabolism,and citrate cycle pathways.

关键词： NAFLD LGZGD untargeted metabolomics glycerophospholipid metabolism citrate cycle

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A microRNA encoded by HSV-1 inhibits a cellular transcriptional repressor of viral immediate early and early genes

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Science China(Life Sciences) 2013年第4期56卷 373-383页

作者： WU WenJuan GUO ZhongPing ZHANG XueMei GUO Lei LIU LongDing LIAO Yun WANG JingJing WANG LiChun LI QiHan Institute of medical Biology Chinese Academy of Medical Sciences Peking Union Medical College first affilliated hospital of kunming medical university Chinese Pharmacopoeia Commission

Viral microRNAs are one component of the RNA interference phenomenon generated during viral infection. They were first identified in the Herpesviridae family, where they were found to regulate viral mRNA translation. In addition, prior work has suggested that Kaposi＇s sarcoma-associated herpesvirus （KSHV） is capable of regulating cellular gene transcription by miRNA. We demonstrate that a miRNA, hsvl-mir-H27, encoded within the genome of herpes simplex virus 1 （HSV-1）, targets the mRNA of the cellular transcriptional repressor Kelch-like 24 （KLHL24） that inhibits transcriptional efficiency of viral imme- diate-early and early genes. The viral miRNA is able to block the expression of KLHL24 in cells infected by HSV-1. Our dis- covery reveals an effective viral strategy for evading host cell defenses and supporting the efficient replication and prolifera- tion of HSV- 1.

关键词： herpes simplex virus I (HSV-1) microRNAs (miRNAs) cellular transcriptional repressor Kelch-like 24

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JNK3 involvement in nerve cell apoptosis and neurofunctional recovery after traumatic brain injury

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Neural Regeneration Research 2013年第16期8卷 1491-1499页

作者： Jiang Long Li Cai Jintao Li Lei Zhang Haiyang Yang Tinghua Wang Department of Neurosurgery First Affiliated Hospital of Kunming Medical University Neuroscience Institute of kunming medical university

Increasing evidence has revealed that the activation of the JNK pathway participates In apoptosis o1 nerve cells and neurological function recovery after traumatic brain injury. However, which genes inI the JNK family are activated and their role in traumatic brain injury remain unclear. Therefore, in this study, in situ end labeling, reverse transcription-PCR and neurological function assessment were adopted to investigate the alteration of JNK1, JNK2 and JNK3 gene expression in cerebral injured rats, and their role in celt apoptosis and neurological function restoration. Results showed that JNK3 expression significantly decreased at 1 and 6 hours and 1 and 7 days post injury, but that JNK1 and JNK2 expression remained unchanged. In addition, the number of apoptotic nerve cells surrounding the injured cerebral cortex gradually reduced over time post injury. The Neurological Severity Scores gradually decreased over 1,3, 5, 14 and 28 days post injury. These findings suggested that JNK3 expression was downregulated at early stages of brain injury, which may be associated with apoptosis of nerve cells. Downregulation of JNK3 expression may promote the recovery of neurological function following traumatic brain injury.

关键词： neural regeneration JNK1 JNK2 JNK3 traumatic brain injury TdT-mediated dUTP nick endlabeling reverse transcription-PCR cell apoptosis neurological function recovery neuroregeneration

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Metabolic remodeling in chronic heart failure

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Journal of Zhejiang university-Science B(Biomedicine & Biotechnology) 2013年第8期14卷 688-695页

作者： Jing WANG Tao GUO Department of Cardiology the First Affiliated Hospital of Kunming Medical University

Although the management of chronic heart failure (CHF) has made enormous progress over the past decades, CHF is still a tremendous medical and societal burden. Metabolic remodeling might play a crucial role in the pathophysiology of CHF. The characteristics and mechanisms of metabolic remodeling remained unclear, and the main hypothesis might include the changes in the availability of metabolic substrate and the decline of metabolic capability. In the early phases of the disease, metabolism shifts toward carbohydrate utilization from fatty acids (FAs) oxidation. Along with the progress of the disease, the increasing level of the hyperadrenergic state and insulin resistance cause the changes that shift back to a greater FA uptake and oxidation. In addition, a growing body of experimental and clinical evidence suggests that the improvement in the metabolic capability is likely to be more significant than the selection of the substrate.

关键词： Chronic heart failure (CHF) Metabolic remodeling Metabolic substrate Metabolic capability

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Melatonin attenuates hepatic ischemia-reperfusion injury in rats by inhibiting NF-κB signaling pathway

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Hepatobiliary & Pancreatic Diseases International 2021年第6期20卷 551-560页

作者： Yao Gao Zhi-Tao Li Li Jin Jie Lin Zheng-Lei Fan Zhong Zeng Han-Fei Huang Organ Transplantation Center the First Affiliated Hospital of Kunming Medical UniversityKunming 650032China

Background:The sterile inflammatory response is one of the key mechanisms leading to hepatic ischemia-reperfusion *** has been shown to prevent organ injuries,but its roles in the inflammatory response after hepatic ischemia-reperfusion injury have not been fully explored,especially in late ischemia-reperfusion *** present study aimed to investigate the roles and possible mechanisms of melatonin in the inflammatory response after hepatic ischemia-reperfusion ***:Sixty Sprague-Dawley rats were randomly divided into a sham group,ischemia-reperfusion injury group(I/R group),and melatonin-treated group(M+I/R group).The rats in the I/R group were subjected to 70%hepatic ischemia for 45 min,followed by 5 or 24 h of *** rats in the M+I/R group were injected with melatonin(10 mg/kg,intravenous injection)15 min prior to ischemia and immediately before *** and samples of ischemic liver lobes were harvested for future analysis,and the 7-day survival rate was assessed after hepatic ischemia-reperfusion ***:In comparison with the I/R group,the M+I/R group showed markedly decreased expression levels of inflammatory cytokines(IL-6 and TNF-α)and numbers of apoptotic hepatocytes(P<0.05).Immunoblotting showed that the expression levels of IL-6,p-NF-κBp65/t-NF-κBp65 and p-IκB-α/t-IκB-αin the M+I/R group were significantly lower than those in the I/R group,and immunofluorescence staining showed that the expression level of p-NF-κBp65 in the M+I/R group was lower than that in the I/R group(P<0.05).The 7-day survival rates were 20%in the I/R group and 50%in the M+I/R group(P<0.05).Conclusions:Melatonin downregulated the activity of the NF-κB signaling pathway in the early and late stages of hepatic ischemia-reperfusion injury,alleviated the inflammatory response,protected the liver from ischemia-reperfusion injury,and increased the survival rate.

关键词： Melatonin Ischemia-reperfusion injury Inflammation NF-κB Liver

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Panax notoginseng saponins improve recovery after spinal cord transection by upregulating neurotrophic factors

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Neural Regeneration Research 2015年第8期10卷 1317-1320页

作者： Bo Wang Yu Li Xuan-peng Li Yang Li Department of Neurosurgery First Affiliated Hospital Kunming Medical University

Saponins extracted from Panax notoginseng are neuroprotective, but the mechanisms underlying this effect remain unclear. In the present study, we established a rat model of thoracic（T10） spinal cord transection, and injected Panax notoginseng saponins（100 mg/kg） or saline 30 minutes after injury. Locomotor functions were assessed using the Basso, Beattie, and Bresnahan（BBB） scale from 1 to 30 days after injury, and immunohistochemistry was carried out in the ventral horn of the spinal cord at 1 and 7 days to determine expression of nerve growth factor（NGF） and brain-derived neurotrophic factor（BDNF）. Our results show that at 7–30 days post injury, the BBB score was higher in rats treated with Panax notoginseng saponins than in those that received saline. Furthermore, at 7 days, more NGF- and BDNF-immunoreactive neurons were observed in the ventral horn of the spinal cord of rats that had received Panax notoginseng saponins than in those that received saline. These results indicate that Panax notoginseng saponins caused an upregulation of NGF and BDNF in rats with spinal cord transection, and improved hindlimb motor function.

关键词： nerve regeneration Panax notoginseng saponins spinal cord injury nerve growth factor brain-derived neurotrophic factor traditional Chinese medicine neural regeneration

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Electroacupuncture in the repair of spinal cord injury:inhibiting the Notch signaling pathway and promoting neural stem cell proliferation

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Neural Regeneration Research 2015年第3期10卷 394-403页

作者： Xin Geng Tao Sun Jing-hui Li Ning Zhao Yong Wang Hua-lin Yu Second Department of Neurosurgery First Affiliated Hospital of Kunming Medical University

Electroacupuncture for the treatment of spinal cord iniury has a good dinical curative effect, but the underlying mechanism is unclear. In our experiments, the spinal cord of adult Sprague-Daw- ley rats was clamped for 60 seconds. Dazhui （GV14） and Mingmen （GV4） acupoints of rats were subjected to electroacupuncture. Enzyme-linked immunosorbent assay revealed that the expres- sion of serum inflammatory factors was apparently downregulated in rat models of spinal cord injury after electroacupuncture. Hematoxylin-eosin staining and immunohistochemistry results demonstrated that electroacupuncture contributed to the proliferation of neural stem cells in rat injured spinal cord, and suppressed their differentiation into astrocytes. Real-time quantitative PCR and western blot assays showed that electroacupuncture inhibited activation of the Notch signaling pathway induced by spinal cord injury. These findings indicate that electroacupuncture repaired the injured spinal cord by suppressing the Notch signaling pathway and promoting the proliferation of endogenous neural stem ceils.

关键词： nerve regeneration spinal cord electroacupuncture therapy neural stem cells notchsignaling pathway astrocytes inflammation survival curve proliferation differentiation real-timequantitative PCR western blot assay neural regeneration

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Emerging role of long noncoding RNAs in recurrent hepatocellular carcinoma

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World Journal of Clinical Cases 2021年第32期9卷 9699-9710页

作者： Yuan Fang Yang Yang Na Li Xiao-Li Zhang Han-Fei Huang Organ Transplantation Center The First Affiliated Hospital of Kunming Medical UniversityKunming 650032Yunnan ProvinceChina Department of Otorhinolaryngology The First Affiliated Hospital of Kunming Medical UniversityKunming 650032Yunnan ProvinceChina Department of Gastrointestinal and Hernia Surgery The First Affiliated Hospital of Kunming Medical UniversityKunming 650032Yunnan ProvinceChina

Hepatocellular carcinoma(HCC)remains one of the most frequent types of liver cancer and is characterized by a high recurrence *** studies have proposed that long non-coding RNAs(lncRNAs)are potential biomarkers in several recurrent tumor *** is now well understood that invasion,migration,and metastasis are important factors for tumor ***,some of the known risk factors for HCC may affect the expression levels of several types of lncRNAs and thus affect the recurrence of liver cancer through lncRNA *** this paper,we review the biological functions,molecular mechanisms,and roles of lncRNAs in HCC and summarize current knowledge about lncRNAs as potential biomarkers in recurrent HCC.

关键词： Long non-coding RNAs Hepatocellular carcinoma Liver cancer Biomarker Recurrence

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Principle of relative positioning of structures in the human body

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Neural Regeneration Research 2013年第9期8卷 853-856页

作者： Buliang Meng Ailan Pang Ming Li Department of Human Anatomy Histology and Embryology Kunming Medical University Department of Neurology First Affiliated Hospital of Kunming Medical University

The arrangement of various biological structures should generally ensure the safety of crucial structures and increase their working efficiency; however, other principles governing the relative positions of structures in humans have not been reported. The present study therefore investigated other principles using nerves and their companion vessels in the human body as an example. Nerves and blood vessels usually travel together and in the most direct way towards their targets. Human embryology, histology, and gross anatomy suggest that there are many possible positions for these structures during development. However, for mechanical reasons, tougher or stronger structures should take priority. Nerves are tougher than most other structures, followed by arteries, veins, and lymphatic vessels. Nerves should therefore follow the most direct route, and be followed by the arteries, veins, and lymphatic vessels. This general principle should be applicable to all living things.

关键词： neural regeneration reviews principle position anatomy human embryology histology neuroregeneration

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Tranylcypromine upregulates Sestrin 2 expression to ameliorate NLRP3-related noise-induced hearing loss

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Neural Regeneration Research 2025年第5期20卷 1483-1494页

作者： Xihang Chen Zhifeng Chen Menghua Li Weiwei Guo Shuolong Yuan Liangwei Xu Chang Lin Xi Shi Wei Chen Shiming Yang Senior Department of Otolaryngology Head and Neck Surgery Chinese PLA General HospitalChinese PLA Medical SchoolBeijingChina State Key Laboratory of Hearing and Balance Science BeijingChina National Clinical Research Center for Otolaryngologic Diseases BeijingChina Key Laboratory of Hearing Science Ministry of EducationBeijingChina Beijing Key Laboratory of Hearing Impairment Prevention and Treatment BeijingChina Department of Otorhinolaryngology Head and Neck Surgery The First Affiliated Hospital of Fujian Medical UniversityFuzhouFujian ProvinceChina Department of Otolaryngology Head and Neck Surgery The 940th Hospital of Joint Logistics Support Force of Chinese PLALanzhouGansu ProvinceChina Key Laboratory of Tropical Biological Resources of Ministry of Education School of Pharmaceutical SciencesHainan UniversityHaikouHainan ProvinceChina Academician Workstation of Hainan university School of Pharmaceutical SciencesYazhou BaySanyaHainan ProvinceChina

Noise-induced hearing loss is the primary non-genetic factor contributing to auditory ***,there are currently no effective pharmacological interventions for patients with noise-induced hearing ***,we present evidence suggesting that the lysine-specific demethylase 1 inhibitor–tranylcypromine is an otoprotective agent that could be used to treat noise-induced hearing loss,and elucidate its underlying regulatory *** established a mouse model of permanent threshold shift hearing loss by exposing the mice to white broadband noise at a sound pressure level of 120 d B for 4 *** found that tranylcypromine treatment led to the upregulation of Sestrin2(SESN2)and activation of the autophagy markers light chain 3B and lysosome-associated membrane glycoprotein 1 in the cochleae of mice treated with *** noise exposure group treated with tranylcypromine showed significantly lower average auditory brainstem response hearing thresholds at click,4,8,and 16 k Hz frequencies compared with the noise exposure group treated with *** findings indicate that tranylcypromine treatment resulted in increased SESN2,light chain 3B,and lysosome-associated membrane glycoprotein 1 expression after noise exposure,leading to a reduction in levels of 4-hydroxynonenal and cleaved caspase-3,thereby reducing noise-induced hair cell ***,immunoblot analysis demonstrated that treatment with tranylcypromine upregulated SESN2 expression via the autophagy *** treatment also reduced the production of NOD-like receptor family pyrin domaincontaining 3(NLRP3)*** conclusion,our results showed that tranylcypromine treatment ameliorated cochlear inflammation by promoting the expression of SESN2,which induced autophagy,thereby restricting NLRP3-related inflammasome signaling,alleviating cochlear hair cell loss,and protecting hearing *** findings suggest that inhibiting lysine-specific demethylase 1 is a

关键词： 4-hydroxynonenal apoptosis autophagy cleaved caspase-3 inflammation NOD-like receptor family pyrin domain-containing 3(NLRP3) noise-induced hearing loss oxidative stress Sestrin2 tranylcypromine

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