ObjectiveTo explore the mechanism of Shenmai injection in improving cisplatin resistance in non-small cell lung cancer （NSCLC） based on the endoplasmic reticulum stress through protein kinase R-like endoplasmic reticulum kinase （PERK）/activated transcription factor 4 （ATF4）/C/EBP homologous protein （CHOP） signaling pathway. MethodsBALB/c nude mice bearing cisplatin-resistant human lung cancer cell line （A549/cisplatin） were randomly divided into four groups： Blank control group （0.9% sodium chloride）， cisplatin group （5 µg·g^-1cisplatin）， Shenmai injection group （5.2 mg·g^-1 Shenmai injection）， and combination therapy group （5.2 mg·g^-1 Shenmai injection +5 µg·g^-1cisplatin）. The drug intervention lasted for 4 weeks， and the changes in body weight and tumor volume were monitored. Hematoxylin-eosin （HE） staining was performed to observe tumor tissue pathology. Transmission electron microscopy （TEM） was used to assess the morphology of the endoplasmic reticulum. Immunohistochemical assay was conducted to measure the positive expressions of PERK， ATF4， and CHOP in tumor tissues. Western blot quantified the protein expression of immunoglobulin heavy chain binding protein （BIP）， PERK， phosphorylated PERK （p-PERK）， eukaryotic translation initiation factor 2α （eIF2α）， phosphorylated eIF2α （p-eIF2α）， ATF4， CHOP， B-cell lymphoma -2 （Bcl-2）， and Bcl-2 Associated X protein （Bax）. A549/cis cells were divided into blank group： Blank control group （normal culture medium）， cisplatin group （23.3 µmol·L^-1 cisplatin）， Shenmai Injection group （20 g·L^-1 Shenmai injection）， and combination therapy group （20 g·L^-1 Shenmai injection+23.3 µmol·L^-1 cisplatin）. Cell counting kit-8 （CCK-8） method was used to detect cell viability， TEM was used to observe the morphology of endoplasmic reticulum， and Western blot was used to detect endoplasmic reticulum stress and apoptosis-related proteins. ResultsCompared with the cisplatin group， the combination therapy group showed increased body weight （P<0.05）， decreased tumor volume （P<0.05）， and expanded endoplasmic reticulum in tumor cells. The positive expressions of PERK， ATF4， and CHOP increased （P<0.05）. Western blot revealed elevated protein expression levels of BIP， p-PERK/PERK， p-eIF2α/eIF2α， ATF4， CHOP， and Bax （P<0.05）， while Bcl-2 expression decreased （P<0.05）. As shown in the in vitro experiment， compared with the cisplatin group， the combination therapy group exhibited a reduced cell survival rate （P<0.05）. TEM revealed increased endoplasmic reticulum dilation and vesicular degeneration. Western blotting showed increased protein levels of BIP， p-PERK/PERK， p-eIF2α/eIF2α， ATF4， CHOP and Bax （P<0.05）， with decreased Bcl-2 expression （P<0.05）. ConclusionShenmai injection combined with cisplatin has a synergistic antitumor effect in NSCLC， which may be attributed to the activation of endoplasmic reticulum stress response mediated by the PERK/eIF2α/ATF4/CHOP signaling pathway and the induction of tumor cell apoptosis.

Background: Breast cancer is a common malignant tumor that has a high tendency to metastasis to the bone, leading to cancer-induced bone pain (CIBP). Ghrelin can not only stimulate appetite and regulate energy balance, but also alleviate CIBP by inducing NPY expression. Octanoic acid (OA), a type of medium chain fatty acids, provides an energy substrate and promotes acylation of ghrelin. However, it remains to be elucidated whether an OA-rich diet can alleviate CIBP by activating the acyl-ghrelin/NPY pathway. Methods: First, thirty-six Sprague–Dawley rats were randomly divided into the sham, CIBP, CIBP + OA (20), CIBP + OA (40), CIBP + OA (60) and CIBP + OA (80) groups to investigate the effects of diets with different ratios of OA on CIBP and the acyl-ghrelin/NPY pathway. Next, a ghrelin O-acyltransferase (GOAT) inhibitor was exogenously administered to investigate whether an OA-rich diet alleviated CIBP through increasing the level of acyl-ghrelin and activating the acyl-ghrelin/NPY pathway. Results: An OA-rich diet significantly alleviated nociceptive behaviors and increased the levels of acyl-ghrelin and NPY in a dose-dependent manner in cancer-bearing rats. With the exogenous administration of the GOAT inhibitor, the beneficial effects of an OA-rich diet on the acyl-ghrelin/NPY pathway and its pain-relieving effects were attenuated. Conclusions An OA-rich diet could alleviate CIBP through increasing the level of acyl-ghrelin and activating the acylghrelin/NPY pathway.

AIM To evaluate the quality of Gegen Formula Granules.METHODS Linear calibration with two reference substances(LCTRS)was adopted in the predicting of retention time with puerarin and daidzein as internal standards.UPLC characteristic chromatograms were established.The contents of 3'-hydroxy puerarin,puerarin(internal standard),3'-methoxy puerarin,puerarin 6"-O-xyloside,puerarin apioside and daidzin were determined by quantitative determination analysis multi-components by a single marker(QAMS),after which their transfer rates were calculated.RESULTS Compared with relative retention time method,LCTRS demonstrated higher positional accuracy for characteristic peaks and wider application range for columns.There were 9 characteristic peaks in the characteristic chromatograms for 14 batches of formula granules and 15 batches of standard decoctions with the similarities of more than 0.95.The contents and transfer rates of various constituents in formula granules and standard decoctions were basically consistent.CONCLUSION The chemical constituents in formula granules and their standard decoctions of Puerariae lobatae Radix display good consistency,reliable preparation process is observable in the former.

Objective To explore the efficacy of ranibizumab combined with retinal laser photocoagulation in patients with macular edema secondary to branch retinal vein occlusion(BRVO)and its impact on best-corrected visual acuity(BCVA)and central macular thickness(CMT).Methods A prospective analysis was conducted on 70 patients with secondary macular edema caused by BRVO who were admitted to the 901th Hospital of Joint Logistics Support Force from March 2019 to March 2023.According to the random number table method,the patients were assigned into study group or control group,with 35 cases in each group.The control group was treated with ranibizumab,while the study group was treated with ranibizumab and retinal laser photocoagulation.The efficacy,BCVA,CMT,intraocular pressure,adverse reactions,and 36-item short form health survey(SF-36)score were compared between the two groups.Results There was a significant difference in the efficacy between the two groups(Z=2.272,P<0.05),and the total effective rate of the study group was higher than that of the control group(P<0.05).The results of repeated measure ANOVA showed that CMT and intraocular pressure decreased significantly,while BCVA increased significantly in both groups after 3 months,6 months,and 12 months of treatment(P<0.05);moreover,these parameters in the study group were superior to those in the control group(P<0.05).There were no significant differences in the incidence of cataracts,transient intraocular pressure elevation,subconjunctival hemorrhage,retinal detachment,or the total incidence of adverse reactions between the two groups(P>0.05).After 12 months of treatment,the total score of SF-36 increased in both groups(P<0.05),and the difference value of total score of SF-36 in the study group was superior to that in the control group(P<0.05).Conclusion The combination of ranibizumab and retinal laser photocoagulation can achieve a good therapeutic effect on macular edema caused by BRVO.It can effectively improve BCVA,CMT and intraocular pressure,reduce the risk of adverse reactions,and enhance the quality of life.

Epilepsy is a chronic neurological disease caused by abnormal synchronous discharge of the brain, which is characterized by recurrent and transient neurological abnormalities, mainly manifested as loss of consciousness and limb convulsions, and can occur in people of all ages. At present, anti-epileptic drugs (AEDs) are still the main means of treatment, but their efficacy is limited by the problem of drug resistance, and long-term use can cause serious side effects, such as cognitive dysfunction and vital organ damage. Although surgical resection of epileptic lesions has achieved certain results in some patients, the high cost and potential risk of neurological damage limit its scope of application. Therefore, the development of safe, accurate and personalized non-invasive treatment strategies has become one of the key directions of epilepsy research. In recent years, photobiomodulation (PBM) has gained significant attention as a promising non-invasive therapeutic approach. PBM uses light of specific wavelengths to penetrate tissues and interact with photosensitive molecules within cells, thereby modulating cellular metabolic processes. Research has shown that PBM can enhance mitochondrial function, promote ATP production, improve meningeal lymphatic drainage, reduce neuroinflammation, and stimulate the growth of neurons and synapses. These biological effects suggest that PBM not only holds the potential to reduce the frequency of seizures but also to improve the metabolic state and network function of neurons, providing a novel therapeutic avenue for epilepsy treatment. Compared to traditional treatment methods, PBM is non-invasive and avoids the risks associated with surgical interventions. Its low risk of significant side effects makes it particularly suitable for patients with drug-resistant epilepsy, offering new therapeutic options for those who have not responded to conventional treatments. Furthermore, PBM’s multi-target mechanism enables it to address a variety of complex etiologies of epilepsy, demonstrating its potential in precision medicine. In contrast to therapies targeting a single pathological mechanism, PBM’s multifaceted approach makes it highly adaptable to different types of epilepsy, positioning it as a promising supplementary or alternative treatment. Although animal studies and preliminary clinical trials have shown positive outcomes with PBM, its clinical application remains in the exploratory phase. Future research should aim to elucidate the precise mechanisms of PBM, optimize light parameters, such as wavelength, dose, and frequency, and investigate potential synergistic effects with other therapeutic modalities. These efforts will be crucial for enhancing the therapeutic efficacy of PBM and ensuring its safety and consistency in clinical settings. This review summarizes the types of epilepsy, diagnostic biomarkers, the advantages of PBM, and its mechanisms and potential applications in epilepsy treatment. The unique value of PBM lies not only in its multi-target therapeutic effects but also in its adaptability to the diverse etiologies of epilepsy. The combination of PBM with traditional treatments, such as pharmacotherapy and neuroregulatory techniques, holds promise for developing a more comprehensive and multidimensional treatment strategy, ultimately alleviating the treatment burden on patients. PBM has also shown beneficial effects on neural network plasticity in various neurodegenerative diseases. The dynamic remodeling of neural networks plays a critical role in the pathogenesis and treatment of epilepsy, and PBM’s multi-target mechanism may promote brain function recovery by facilitating neural network remodeling. In this context, optimizing optical parameters remains a key area of research. By adjusting parameters such as wavelength, dose, and frequency, researchers aim to further enhance the therapeutic effects of PBM while maintaining its safety and stability. Looking forward, interdisciplinary collaboration, particularly in the fields of neuroscience, optical engineering, and clinical medicine, will drive the development of PBM technology and facilitate its transition from laboratory research to clinical application. With the advancement of portable devices, PBM is expected to provide safer and more effective treatments for epilepsy patients and make a significant contribution to personalized medicine, positioning it as a critical component of precision therapeutic strategies.

Background: Breast cancer is a common malignant tumor that has a high tendency to metastasis to the bone, leading to cancer-induced bone pain (CIBP). Ghrelin can not only stimulate appetite and regulate energy balance, but also alleviate CIBP by inducing NPY expression. Octanoic acid (OA), a type of medium chain fatty acids, provides an energy substrate and promotes acylation of ghrelin. However, it remains to be elucidated whether an OA-rich diet can alleviate CIBP by activating the acyl-ghrelin/NPY pathway. Methods: First, thirty-six Sprague–Dawley rats were randomly divided into the sham, CIBP, CIBP + OA (20), CIBP + OA (40), CIBP + OA (60) and CIBP + OA (80) groups to investigate the effects of diets with different ratios of OA on CIBP and the acyl-ghrelin/NPY pathway. Next, a ghrelin O-acyltransferase (GOAT) inhibitor was exogenously administered to investigate whether an OA-rich diet alleviated CIBP through increasing the level of acyl-ghrelin and activating the acyl-ghrelin/NPY pathway. Results: An OA-rich diet significantly alleviated nociceptive behaviors and increased the levels of acyl-ghrelin and NPY in a dose-dependent manner in cancer-bearing rats. With the exogenous administration of the GOAT inhibitor, the beneficial effects of an OA-rich diet on the acyl-ghrelin/NPY pathway and its pain-relieving effects were attenuated. Conclusions An OA-rich diet could alleviate CIBP through increasing the level of acyl-ghrelin and activating the acylghrelin/NPY pathway.

ObjectiveTo investigate the mechanism of liver injury induced by tripterygium glycosides tablets （TG） and the molecular mechanism of compound glycyrrhizin tablets （CG） in alleviating the abnormalities of cholesterol metabolism caused by TG via cholesterol metabolism. MethodsAccording to the body weights， male Sprague-Dawley （SD） rats were randomly grouped as follows： control （pure water）， low-dose TG （TG-L， 189.0 mg·kg^-1·d^-1）， high-dose TG （TG-H， 472.5 mg·kg^-1·d^-1）， TG-L+CG （189.0 mg·kg^-1·d^-1 TG + 20.25 mg·kg^-1·d^-1 CG）， and TG-H+CG （472.5 mg·kg^-1·d^-1 TG + 20.25 mg·kg^-1·d^-1 CG）， with 6 rats in each group. Rats were administrated with corresponding drugs once daily for 3 weeks. At the end of the last administration， the mRNA and protein levels of liver X receptor-alpha （LXR-α）， low-density lipoprotein receptor （LDLR）， adenosine triphosphate-binding cassette transporter A1 （ABCA1）， adenosine triphosphate-binding cassette transporter G1 （ABCG1）， 3-hydroxy-3-methylglutaryl coenzyme A reductase （HMGCR）， cholesterol 7α-hydroxylase （CYP7A1）， cholesterol 12α-hydroxylase （CYP8B1）， and sterol 27-hydroxylase （CYP27A1） in the liver tissue were determined by Real-time PCR and Western blotting， respectively. The level of 3-hydroxy-3-methylglutaryl coenzyme A reductase （HMG-CoAR）， a regulatory enzyme of cholesterol synthesis， was measured by enzyme-linked immunosorbent assay （ELISA）. HepG2 cells were used to observe the effect of TG on the cell proliferation in vitro. Specifically， HepG2 cells were grouped as follows： Low-dose TG （TG-l， 15 mg·L^-1）， medium-dose TG （TG-m， 45 mg·L^-1）， high-dose TG （TG-h， 135 mg·L^-1）， fenofibrate （FB， 10 μmol·L^-1）， CG extract， TG-h+FB （135 mg·L^-1 TG + 10 μmol·L^-1 FB）， TG-m+FB （45 mg·L^-1 TG + 10 μmol·L^-1 FB）， TG-l+FB （15 mg·L^-1 TG + 10 μmol·L^-1 FB）， TG-h+CG （135 mg·L^-1 TG + 60 μmol·L^-1 CG）， TG-m+CG （45 mg·L^-1 TG + 60 μmol·L^-1 CG）， and TG-l+CG （15 mg·L^-1 TG + 60 μmol·L^-1 CG）. The mRNA and protein levels of LXR-α， ABCG1， LDLR， CYP7A1， CYP8B1， and CYP27A1 in HepG2 cells were determined by Real-time PCR and Western blotting， respectively. ResultsThe rat experiment showed that compared with the control group， the TG-H group showed down-regulated mRNA levels of CYP7A1， CYP8B1， and CYP27A1 in the liver tissue （P<0.05， P<0.01）， which were up-regulated by the application of CG （P<0.05， P<0.01）， and the TG-H+CG group showed up-regulated mRNA level of LDLR （P<0.01）. Compared with the control group， the TG-L and TG-H groups showed down-regulated protein levels of LDLR， CYP7A1， and CYP8B1 in the liver tissue （P<0.05， P<0.01）. In addition， the protein levels of ABCG1 and LXR-α were down-regulated in the TG-H and TG-L groups， respectively （P<0.05）. Compared with TG alone， TG+CG up-regulated the protein levels of ABCG1 and LDLR （P<0.05， P<0.01）， and the protein levels of CYP7A1 and CYP8B1 in the TG-H+CG group were up-regulated （P<0.05， P<0.01）. The cell experiment showed that compared with the control group， the TG-h group presented up-regulated mRNA level of LXR-α （P<0.01）， and the TG-m and TG-h groups showcased down-regulated mRNA levels of LDLR and CYP7A1 （P<0.01） and up-regulated mRNA level of CYP27A1 （P<0.01） in HepG2 cells. The combination of CG with TG restored the above changes （P<0.01）. Western blotting results showed that compared with the control group， the TG-m and TG-h groups showed down-regulated protein levels of LXR-α， ABCG1， LDLR， CYP7A1， CYP8B1， and CYP27A1 in HepG2 cells （P<0.01）. Compared with the TG-h group， the TG-h+CG group showed up-regulated protein level of LDLR （P<0.05）. Compared with the TG-m group， the TG-m+CG group showcased up-regulated protein levels of LDLR， ABCG1， CYP7A1， and CYP27A1 （P<0.05， P<0.01）. ConclusionThe administration of TG at 189.0， 472.5 mg·kg^-1 for 3 weeks could modulate the signaling pathways associated with cholesterol efflux， endocytosis， and cholesterol biotransformation in hepatocytes， leading to the accumulation of cholesterol and subsequent liver injury in rats. CG could ameliorate the liver injury induced by lipid metabolism disorders caused by TG by up-regulating the expression of LXR-α， LDLR， ABCG1， CYP7A1， CYP8B1， and CYP27A1 to promote cholesterol biotransformation.

Background: Breast cancer is a common malignant tumor that has a high tendency to metastasis to the bone, leading to cancer-induced bone pain (CIBP). Ghrelin can not only stimulate appetite and regulate energy balance, but also alleviate CIBP by inducing NPY expression. Octanoic acid (OA), a type of medium chain fatty acids, provides an energy substrate and promotes acylation of ghrelin. However, it remains to be elucidated whether an OA-rich diet can alleviate CIBP by activating the acyl-ghrelin/NPY pathway. Methods: First, thirty-six Sprague–Dawley rats were randomly divided into the sham, CIBP, CIBP + OA (20), CIBP + OA (40), CIBP + OA (60) and CIBP + OA (80) groups to investigate the effects of diets with different ratios of OA on CIBP and the acyl-ghrelin/NPY pathway. Next, a ghrelin O-acyltransferase (GOAT) inhibitor was exogenously administered to investigate whether an OA-rich diet alleviated CIBP through increasing the level of acyl-ghrelin and activating the acyl-ghrelin/NPY pathway. Results: An OA-rich diet significantly alleviated nociceptive behaviors and increased the levels of acyl-ghrelin and NPY in a dose-dependent manner in cancer-bearing rats. With the exogenous administration of the GOAT inhibitor, the beneficial effects of an OA-rich diet on the acyl-ghrelin/NPY pathway and its pain-relieving effects were attenuated. Conclusions An OA-rich diet could alleviate CIBP through increasing the level of acyl-ghrelin and activating the acylghrelin/NPY pathway.

Background: Breast cancer is a common malignant tumor that has a high tendency to metastasis to the bone, leading to cancer-induced bone pain (CIBP). Ghrelin can not only stimulate appetite and regulate energy balance, but also alleviate CIBP by inducing NPY expression. Octanoic acid (OA), a type of medium chain fatty acids, provides an energy substrate and promotes acylation of ghrelin. However, it remains to be elucidated whether an OA-rich diet can alleviate CIBP by activating the acyl-ghrelin/NPY pathway. Methods: First, thirty-six Sprague–Dawley rats were randomly divided into the sham, CIBP, CIBP + OA (20), CIBP + OA (40), CIBP + OA (60) and CIBP + OA (80) groups to investigate the effects of diets with different ratios of OA on CIBP and the acyl-ghrelin/NPY pathway. Next, a ghrelin O-acyltransferase (GOAT) inhibitor was exogenously administered to investigate whether an OA-rich diet alleviated CIBP through increasing the level of acyl-ghrelin and activating the acyl-ghrelin/NPY pathway. Results: An OA-rich diet significantly alleviated nociceptive behaviors and increased the levels of acyl-ghrelin and NPY in a dose-dependent manner in cancer-bearing rats. With the exogenous administration of the GOAT inhibitor, the beneficial effects of an OA-rich diet on the acyl-ghrelin/NPY pathway and its pain-relieving effects were attenuated. Conclusions An OA-rich diet could alleviate CIBP through increasing the level of acyl-ghrelin and activating the acylghrelin/NPY pathway.

Background: Breast cancer is a common malignant tumor that has a high tendency to metastasis to the bone, leading to cancer-induced bone pain (CIBP). Ghrelin can not only stimulate appetite and regulate energy balance, but also alleviate CIBP by inducing NPY expression. Octanoic acid (OA), a type of medium chain fatty acids, provides an energy substrate and promotes acylation of ghrelin. However, it remains to be elucidated whether an OA-rich diet can alleviate CIBP by activating the acyl-ghrelin/NPY pathway. Methods: First, thirty-six Sprague–Dawley rats were randomly divided into the sham, CIBP, CIBP + OA (20), CIBP + OA (40), CIBP + OA (60) and CIBP + OA (80) groups to investigate the effects of diets with different ratios of OA on CIBP and the acyl-ghrelin/NPY pathway. Next, a ghrelin O-acyltransferase (GOAT) inhibitor was exogenously administered to investigate whether an OA-rich diet alleviated CIBP through increasing the level of acyl-ghrelin and activating the acyl-ghrelin/NPY pathway. Results: An OA-rich diet significantly alleviated nociceptive behaviors and increased the levels of acyl-ghrelin and NPY in a dose-dependent manner in cancer-bearing rats. With the exogenous administration of the GOAT inhibitor, the beneficial effects of an OA-rich diet on the acyl-ghrelin/NPY pathway and its pain-relieving effects were attenuated. Conclusions An OA-rich diet could alleviate CIBP through increasing the level of acyl-ghrelin and activating the acylghrelin/NPY pathway.