Cytoglobin(Cygb)is a recently discov-ered astrocyte specific globin that is widely distrib-uted in mammalian visceral organs such as the lung,heart,spleen,liver,pancreas,stomach,small intestine,kidney,neuron,and bone tissue.It plays an important role in clearing reactive oxygen spe-cies,nitric oxide and nitrite signal transduction,al-leviating oxidative stress,anti-fibrosis,regulation of cell apoptosis and treatment of cancer,etc.It is worth noting that the anti-fibrosis role of Cygb has attracted increasing attention in recent years.The existing research has involved various fibrotic dis-eases such as the liver,pancreas,kidney,spleen,etc.,especially in the study of liver fibrosis,which has made great progress.This article system re-views the role of Cygb in various fibrotic diseases,with a focus on its mechanism of alleviating oxida-tive stress.Although the application of Cygb in fi-brotic diseases is still in its infancy and the underly-ing mechanisms still require extensive research and exploration,there is no doubt that Cygb can serve as a promising therapeutic target,with the poten-tial to be widely used in the prevention and treat-ment of fibrotic diseases.

Objective The quality of compound menthol nasal drops was reviewed and analyzed,and identified the bad trend in time.The improvement measures were formulated to improve the quality of the preparation.Methods Taking camphor and menthol in compound menthol nasal drops of Beijing Shijitan Hospital,Capital Medical University,as indicators,the quality of 30 batches of samples was retrospectively analyzed using the capacity sixpack report.The failure mode and effect analysis(FMEA)were applied to the prospective quality risk management.Results All 30 batches of compound menthol nasal drops met the quality standards,and the process was under control.Howe ver,there were potential risks in the process of menthol,so risk management was carried out and improvement measures are formulated.Conclusion The compound menthol nasal drops of the hospital have stable quality,and the quality of the medicine can be continuously ensured with improved processes.

OBJECTIVES: To explore the effects of cannabidiol on endoplasmic reticulum stress and neuronal apoptosis in rats with multiple concussions (MCC). METHODS: SD rats were randomized into sham group, MCC group, 1% tween20 (TW) treatment group, and low-dose (10 mg/kg) and high-dose (40 mg/kg) cannabidiol treatment groups. In all but the sham group, MCC models were established using a metal pendulum percussion device, after which the rats received daily intraperitoneal injections of the corresponding agents for 2 weeks. The expressions of PERK, eIF2α, ATF4, CHOP, TRIB3, p-Akt and pro-caspase-3 in the brain tissue of the rats were detected with qRT-PCR, Western blotting and immunofluorescence staining. The core targets of cannabidiol in treatment of traumatic brain injury (TBI) were identified by network pharmacology analysis, and molecular docking was carried out to simulate the interaction of cannabidiol with the factors related to endoplasmic reticulum stress and apoptosis. RESULTS: Compared with the sham-operated rats, the rat models of MCC showed significantly increased mRNA expressions of PERK, eIF2α and CHOP and protein expressions of PERK, eIF2α, ATF4, CHOP, TRIB3, p-AKT and pro-caspase-3 in the cerebral cortex. CBD treatment, especially at the high dose, obviously increased the expression of p-Akt and lowered the expression levels of the other factors tested in the rat models. Network pharmacology analysis indicated interactions of the core targets of CBD with the factors related to endoplasmic reticulum stress and TBI, and molecular docking study showed a high binding energy of CBD with multiple factors pertaining to endoplasmic reticulum stress and apoptosis. CONCLUSIONS MCC induce endoplasmic reticulum stress and apoptosis in rat brain tissues, for which CBD, especially at a high dose, provides neuroprotective effects by inhibiting endoplasmic reticulum stress and cell apoptosis.
Animals ; Endoplasmic Reticulum Stress/drug effects* ; Apoptosis/drug effects* ; Rats, Sprague-Dawley ; Activating Transcription Factor 4/metabolism* ; Transcription Factor CHOP/metabolism* ; Rats ; Eukaryotic Initiation Factor-2/metabolism* ; Signal Transduction/drug effects* ; eIF-2 Kinase/metabolism* ; Cannabidiol/pharmacology* ; Neurons/metabolism* ; Brain Concussion/metabolism* ; Male ; Molecular Docking Simulation

Objective The quality of compound menthol nasal drops was reviewed and analyzed,and identified the bad trend in time.The improvement measures were formulated to improve the quality of the preparation.Methods Taking camphor and menthol in compound menthol nasal drops of Beijing Shijitan Hospital,Capital Medical University,as indicators,the quality of 30 batches of samples was retrospectively analyzed using the capacity sixpack report.The failure mode and effect analysis(FMEA)were applied to the prospective quality risk management.Results All 30 batches of compound menthol nasal drops met the quality standards,and the process was under control.Howe ver,there were potential risks in the process of menthol,so risk management was carried out and improvement measures are formulated.Conclusion The compound menthol nasal drops of the hospital have stable quality,and the quality of the medicine can be continuously ensured with improved processes.

Cytoglobin(Cygb)is a recently discov-ered astrocyte specific globin that is widely distrib-uted in mammalian visceral organs such as the lung,heart,spleen,liver,pancreas,stomach,small intestine,kidney,neuron,and bone tissue.It plays an important role in clearing reactive oxygen spe-cies,nitric oxide and nitrite signal transduction,al-leviating oxidative stress,anti-fibrosis,regulation of cell apoptosis and treatment of cancer,etc.It is worth noting that the anti-fibrosis role of Cygb has attracted increasing attention in recent years.The existing research has involved various fibrotic dis-eases such as the liver,pancreas,kidney,spleen,etc.,especially in the study of liver fibrosis,which has made great progress.This article system re-views the role of Cygb in various fibrotic diseases,with a focus on its mechanism of alleviating oxida-tive stress.Although the application of Cygb in fi-brotic diseases is still in its infancy and the underly-ing mechanisms still require extensive research and exploration,there is no doubt that Cygb can serve as a promising therapeutic target,with the poten-tial to be widely used in the prevention and treat-ment of fibrotic diseases.

Objective:To investigate the effects of cannabidiol(CBD)on the NOD-like receptor protein 3(NLRP3)inflammasome in the brains of rats with multiple cerebral concussions(MCC).Methods:Rats were subjec-ted to the MCC model and divided into Sham,MCC,vehicle(MCC+TW),CBD-L(10 mg/kg),and CBD-H(40 mg/kg)groups.Immunofluorescence double staining was used to observe changes in NLRP3 and microglial cells in the brain,and Western Blot was performed to detect the expression changes of the NLRP3 inflammasome.Results:A sig-nificant increase in lectin-positive microglial cells of the cortex with enlarged cell bodies and elevated immunofluores-cence intensity of NLRP3 in the activated microglial cells was revealed by immunofluorescence double staining following MCC(P＜0.05).The immunofluorescence intensity of NLRP3 in the activated microglial cells was downregulated by the administration of CBD,with a more pronounced effect observed in the CBD-H group compared to the CBD-L group(P＜0.05).The expression of NLRP3,caspase-1,and apoptosis-associated speck-like protein(ASC)in the cortex,hippocampus,and basal ganglia of rats following MCC was significantly increased,as shown by Western Blot analysis(P＜0.05),and cortical areas are more elevated.The expression of these proteins in different brain regions was reduced by CBD-10 and CBD-40 intervention(P＜0.05).Conclusion:Cannabidiol can reduce the inflammatory response of multiple cerebral concussions rats through NLRP3 inflammasome and protect nerve tissue.

Objective:To explore the impact of scutellarin on the levels of phosphatidylinositol 3-kinase(P13K)and phosphorylated P13K(p-PI3K)in activated microglia.Methods:A rat cerebral ischemia model was made by middle cerebral artery occlusion(MCAO)method.SD rats were randomly divided into three groups:sham operation group(Sham),cerebral ischemia group(MCAO),and cerebral ischemia with scutellarin group(MCAO+S).A model of ischemia-hypoxia injury of BV2 microglia was established by glucose-oxygen deprivation(OGD)and randomly assigned as control group(Control),OGD group and OGD+scutellarin group(OGD+S).Changes in PI3K and p-PI3K expres-sion in microglia were assessed using double immunofluorescence staining and Western Blot.Results:Immunofluores-cence staining and Western Blot analyses revealed a significant increase in p-PI3K levels in activated microglia both in vivo and in vitro(P＜0.05).Furthermore,treatment with scutellarin led to a further elevation in p-PI3K(P＜0.05).However,there were no significant alterations observed in PI3 K expression among the groups(P＞0.05).Conclusion:Scutellarin may play a positive role in the treatment of cerebral ischemia by up-regulating the phosphorylation level of P13K in activated microglia.

Chronic pancreatitis(CP)is a progressive fibroinflammatory disease characterized by destruction of pancreatic aci-nar cells,infiltration of inflammatory cells,activation of pancreatic stellate cell(PSC),and pancreatic fibrosis.Autophagy partici-pates in the maintenance of cell homeostasis.Recent studies have shown that autophagy closely related to the occurrence and develop-ment of CP.However,several autophagy types in the pancreatic microenvironment play different roles in the progression of CP.The autophagy of acinar cells has a"double-edged sword"effect.PSC autophagy is positively correlated with its activation,while the role of autophagy of inflammatory cells is still unclear.This study focused on some key cells in the CP microenvironment and explored the role and mechanism of autophagy in the progression of CP.

ObjectiveTo learn the epidemiological features of foodborne diseases， and to provide scientific basis for disease control. MethodsThe monitoring data of foodborne diseases in Minhang from 2016 to 2020 were analyzed. Stool or swab specimens were collected to detect salmonella， Vibrio parahaemolyticus， Escherichia coli， Shigella， Campylobacter jejuni and norovirus. ResultsThe information of15 951 foodborne disease cases and 11 176 samples were collected， with the positive rate of 12.03%.The cases with diarrhea accounted for 99.90% of the total. The cases with fever accounted for 14.70% of the total. The cases with water stool accounted for 89.70% of the total. May to October were the epidemic periods of foodborne diseases in Minhang（79.78%）. The detection rate was the highest in the 30‒39 age group and cadre staff occupation（13.53%，13.49%）. The detection rates of foodborne bacteria and virus were 5.39% （Vibrio parahaemolyticus）， 3.25% （salmonella），1.44% （norovirus）， 1.06%（Escherichia coli）， 0.56% （Campylobacter jejuni）， 0.34% （mixed infection） and 0% （Shigella）. During this 5-year period， the positive rate of Vibrio parahaemolyticus decreased significantly， while the positive rate of salmonella and Escherichia coli and Campylobacter jejuni increased significantly. The main suspected food were aquatic products （29.44%）， meat （25.80%） and fruits （10.78%）. The main processing methods of suspected food were family workshop （41.12%） and restaurants （37.55%）. The total detection rate of the cases was the highest in the canteen， reaching 20.51%. ConclusionFoodborne disease cases have a seasonal peak. The positive detection of pathogens tends to be similar year by year. The main suspected food is aquatic products. The main resources of suspected food are family workshop， restaurants， and canteen. Targeted health education， supervision and management should be taken to prevent the occurrence of foodborne diseases and the outbreak of food poisoning

Vincristine, a widely used chemotherapeutic agent for treating different cancer, often induces severe peripheral neuropathic pain. A common symptom of vincristine-induced peripheral neuropathic pain is mechanical allodynia and hyperalgesia. However, mechanisms underlying vincristine-induced mechanical allodynia and hyperalgesia are not well understood. In the present study, we show with behavioral assessment in rats that vincristine induces mechanical allodynia and hyperalgesia in a PIEZO2 channel-dependent manner since gene knockdown or pharmacological inhibition of PIEZO2 channels alleviates vincristine-induced mechanical hypersensitivity. Electrophysiological results show that vincristine potentiates PIEZO2 rapidly adapting (RA) mechanically-activated (MA) currents in rat dorsal root ganglion (DRG) neurons. We have found that vincristine-induced potentiation of PIEZO2 MA currents is due to the enhancement of static plasma membrane tension (SPMT) of these cells following vincristine treatment. Reducing SPMT of DRG neurons by cytochalasin D (CD), a disruptor of the actin filament, abolishes vincristine-induced potentiation of PIEZO2 MA currents, and suppresses vincristine-induced mechanical hypersensitivity in rats. Collectively, enhancing SPMT and subsequently potentiating PIEZO2 MA currents in primary afferent neurons may be an underlying mechanism responsible for vincristine-induced mechanical allodynia and hyperalgesia in rats. Targeting to inhibit PIEZO2 channels may be an effective analgesic method to attenuate vincristine-induced mechanical hypersensitivity.