Diallyl trisulfide and its active metabolite allyl methyl sulfone attenuate cisplatin-induced nephrotoxicity by inhibiting the ROS/MAPK/NF-κB pathway.

Cisplatin, a chemotherapy medication employed in the treatment of various solid tumors, is constrained in its clinical application due to nephrotoxicity. Diallyl trisulfide (DATS), a compound derived from garlic that possessed anticancer and antioxidant properties, can be combined with cisplatin without hindering its antitumor effects. The present investigation examined the defensive properties of DATS and its active metabolites against renal dysfunction caused by cisplatin. We created a mouse model to study renal injury caused by cisplatin and assessed kidney histology, immunochemistry, and serum cytokines. DATS treatment effectively reduced the pathological changes caused by cisplatin by decreasing the levels of renal function markers BUN, CRE, cystatin C, NGAL, inflammatory factors TNF-α, IL-6, and the protein expression of α-SMA, NF-κB, KIM-1. A pharmacokinetic evaluation of DATS found that allyl methyl sulfone (AMSO2) was the most abundant and persistent metabolite of DATS in vivo. Then, we examined the impact of AMSO2 on cell viability, apoptosis, ROS generation, and MAPK/NF-κB pathways in HK-2 cells treated with cisplatin. Cotreatment with AMSO2 effectively hindered the HK-2 cells alterations induced by cisplatin. Furthermore, AMSO2 mitigated oxidative stress through the modulation of MAPK and NF-κB pathways. Our findings indicated that DATS and its active derivative AMSO2 attenuated cisplatin-induced nephrotoxicity. DATS shows potential as a viable treatment for nephrotoxicity caused by cisplatin.

Prediction of the mechanism for the combination of diallyl trisulfide and cisplatin against gastric cancer: a network pharmacology study and pharmacological evaluation.

Background: In this research, we aimed to explore the efficacy of diallyl trisulfide (DATS) combined with cisplatin (DDP) for gastric cancer treatment and its underlying mechanism based on network pharmacology. Methods: First, the pharmacological mechanism by which DATS combined with DDP acts against gastric cancer was predicted using network pharmacology. The TTD, GeneCards, and OMIM databases were used to extract drug and disease targets. The David Bioinformatics Resources 6.8 database was used to conduct GO and KEGG analyses. We investigated the efficacy of DATS combined with DDP against gastric cancer in SGC7901 cells and a xenograft model. Furthermore, the specific mechanism of DATS combined with DDP, inferred by network pharmacology, was identified by Western blotting and immunohistochemistry. Results: The combination of DDP and DATS significantly increased cytotoxicity and cell apoptosis compared to the DATS or DDP treatment group in vitro. In addition, continuous intraperitoneal injection of DATS markedly improved the tumor inhibitory effect of DDP in the SGC-7901 tumor-bearing mouse model. Furthermore, network pharmacology and experimental validation studies revealed that the combination of DATS and DDP synergistically enhanced antitumor activity by regulating endoplasmic reticulum stress and inhibiting STAT3/PKC-δ and MAPK signaling pathways. Conclusion: Our study showed that the combination of DATS and DDP could exert outstanding therapeutic effects in gastric cancer. Moreover, network pharmacology coupled with experimental validation revealed the molecular mechanisms of combination therapy for gastric cancer. This study offers a new adjuvant strategy based on DATS and DDP for the treatment of gastric cancer.

Flexible Hollow Core Fiber Photoacoustic Gas Sensor Based on Embedded Acoustic Resonant Structure.

In this paper, we demonstrate a flexible leaky hollow core fiber (LHCF) photoacoustic (PA) gas sensor based on an embedded acoustic resonant structure. The sensor employs a part of a gas conduit as the buffer chamber to construct an equivalent T-type half-open PA cell. The LHCF is installed inside of the gas conduit and the LHCF is hence replaceable. Also, the flexibility of the LHCF and the gas conduit make the gas sensor flexible to reduce spatial size. The inner diameter and length of the LHCF are 1.6 mm and 70 mm, respectively. The inner diameter and length of the gas conduit are 4 mm and 210 mm, respectively. The total gas volume of the sensor is only ∼2.6 mL. Trace acetylene (C2H2) is selected as the target gas to evaluate the performance of the PA gas sensor. A near-infrared distributed feedback (DFB) laser is utilized to generate the PA signal, and an electrical micro-electro-mechanical system (MEMS) microphone is employed to extract the PA signal. The experimental results show that the minimum detection limit (MDL) can be as low as 21.1 ppb when the lock-in integration time is 200 s. And the normalized noise equivalent absorption coefficient (NNEA) is calculated to be 5.7 × 10-9·W/cm-1·Hz-1/2.

Highly sensitive photoacoustic gas sensor with micro-embedded acoustic resonator for gas leakage detection.

In this work, a photoacoustic (PA) gas sensor with a micro-embedded acoustic resonator for gas leakage detection was demonstrated. The micro-embedded acoustic resonator was fabricated by putting a leaky hollow-core fiber (L-HCF) into a cylindrical buffer chamber. The L-HCF was utilized as the PA cavity and the light transmission media simultaneously. The optimal inner diameter of the L-HCF was 1.7 mm. The embedded acoustic resonator was experimentally proven to be equivalent to a T-type half-open acoustic resonator, but the structure became much more compact. The volume of the amount of gas in the cell was only ∼0.3 mL, and the gas diffusion time to fill the sensor under room temperature (25°C) and ambient pressure (101 kPa) was ∼44 s. Trace acetylene (C2H2) in pure nitrogen (N2) was chosen as the target gas, and the minimum detectable limit (MDL) reached 29 ppb when the lock-in integration time was 1 s. The normalized noise equivalent absorption (NNEA) coefficient was calculated to be 3.0 × 10-9 W·cm-1·Hz-1/2. The micro-resonant PA gas sensor, with merits of compactness, low gas consumption, and low cost, has the potential to be a remote gas sensing scheme in fields of environmental protection, industrial process monitoring, and so on.

Low-frequency Resonant Photoacoustic Gas Sensor by Employing Hollow Core Fiber-Based O-Shaped Multipass Cells.

A low-frequency flexible resonant photoacoustic (PA) gas sensor using an O-shaped multipass cell is demonstrated. The PA sensor employed a flexible gradually tapered leaky hollow core fiber (LHCF). The LHCF was bent to be an end-to-end structure to make full use of the incident light. Additionally, the two ends of the LHCF were put inside a single buffer chamber, yielding an equivalent H-type acoustic resonator. The geometric size was reduced thanks to the bending structure. The geometric length of the LHCF was 500 mm. A micro-electro-mechanical-systems electrical microphone was installed at the center of the resonant tube to detect the PA signal. The proposed PA gas sensor exhibited a first-order longitudinal resonance frequency of 408 Hz. Trace acetylene (C2H2) was used as the target gas. The minimum detectable limit was calculated to be 25.8 parts-per-billion (ppb) with an average time of 400 s, which was 1.93 times higher than that of a single-pass PA gas sensor. The normalized noise-equivalent absorption coefficient and the PA cell constant were calculated to be 9.6 × 10-9 W·cm-1·Hz-1/2 and 8295 Pa/W·cm-1, respectively. The PA gas sensor owns a low resonance frequency and can be used for detection of most of the polar gaseous molecules, especially suitable for gas molecules with a long V-T relation time, such as carbon monoxide and carbon dioxide.

CH4, C2H6, and CO2 Multi-Gas Sensing Based on Portable Mid-Infrared Spectroscopy and PCA-BP Algorithm.

A multi-gas sensing system was developed based on the detection principle of the non-dispersive infrared (NDIR) method, which used a broad-spectra light source, a tunable Fabry-Pérot (FP) filter detector, and a flexible low-loss infrared waveguide as an absorption cell. CH4, C2H6, and CO2 gases were detected by the system. The concentration of CO2 could be detected directly, and the concentrations of CH4 and C2H6 were detected using a PCA-BP neural network algorithm because of the interference of CH4 and C2H6. The detection limits were achieved to be 2.59 ppm, 926 ppb, and 114 ppb for CH4, C2H6, and CO2 with an averaging time of 429 s, 462 s, and 297 s, respectively. The root mean square error of prediction (RMSEP) of CH4 and C2H6 were 10.97 ppm and 2.00 ppm, respectively. The proposed system and method take full advantage of the multi-component gas measurement capability of the mid-infrared broadband source and achieve a compromise between performance and system cost.

Fleck-like lesions in CEP290-associated leber congenital amaurosis: a case series.

PURPOSE: To provide a detailed ophthalmic phenotype of a small cohort of patients with Leber Congenital Amaurosis (LCA) caused by mutations in CEP290 (CEP290-LCA) with a focus on elucidating the origin of yellow-white lesions observed in 30% of patients with this condition. METHODS: This is a retrospective review of records of five patients with CEP290-LCA. Patients had comprehensive ophthalmic evaluations. Visual function was assessed with full-field electroretinograms (ffERGs) and full-field sensitivity testing (FST). Multimodal imaging was performed with spectral domain optical coherence tomography (SD-OCT), fundus autofluorescence (FAF) with short- (SW) and near-infrared (NIR) excitation wavelengths. RESULTS: All patients showed relative structural preservation of the foveal and near midperipheral retina separated by a pericentral area of photoreceptor loss. Yellow-white, fleck-like lesions in an annular distribution around the near midperiphery co-localized with hyperreflective lesions on SD-OCT. The lesions located between the inner segment ellipsoid signal and the apical retinal pigment epithelium (RPE). The inner retina was normal. Longitudinal observations in one of the patients indicates the abnormalities may represent an intermediate stage in the degenerative process between the near normal appearing retina previously documented in young CEP290-LCA patients and the pigmentary retinopathy observed along the same region in older individuals. CONCLUSIONS: We speculate that fleck-like lesions in CEP290-LCA correspond to malformed, rudimentary or degenerated, including shed, photoreceptor outer segments. The topography and possible origin of the abnormalities may inform the planning of evolving genetic therapies for this disease.

Spinal Cord Stimulation Improved Freezing of Gait and Hypokinetic Dysarthria of a Patient with Dopamine-Resistant Multiple System Atrophy-Parkinsonian Type.

Background: Multiple system atrophy parkinsonian type (MSA-P) patients with resistance to dopamine have highly limited treatment options. This calls for further study of spinal cord stimulation (SCS) as a potential nondopaminergic therapy to improve motor and speech functions of patients with dopamine-resistant parkinsonism. Case Presentation: A 58-year-old male with MSA-P had hypokinetic dysarthria, freezing of gait (FOG), and spinal disc herniation with refractory back pain. SCS was used to treat his refractory back pain. Serendipitously, after the surgery, the patient reported not only a reduction in pain but also rapid improvement of FOG and hypokinetic dysarthria. Conclusion: SCS has been found in some cases to improve FOG and hypokinetic dysarthria. It is necessary to further study the potential of and the mechanism behind SCS as a potential nondopaminergic therapy to improve motor and speech functions of patients with dopamine-resistant parkinsonism.

Artesunate induces ferroptosis via modulation of p38 and ERK signaling pathway in glioblastoma cells.

Ferroptosis is implicated in various tumors, including glioblastoma. Artesunate (ART), an anti-malarial drug, exerted antitumor properties in several cancer types. However, the role of ferroptosis in the inhibiting effect of artesunate on glioblastoma remains unclear. The purpose of this study was to investigate the effects of ART on the ferroptosis of glioblastoma and to elucidate the underlying mechanisms. We found that ART inhibited the proliferation of glioblastoma cells in vitro and glioblastoma tumorigenesis in vivo. Characteristic changes of ferroptosis were observed in ART group, including GSH depletion, lipid peroxidation and iron overload. Meanwhile, the protein level of GPX4 were lower in ART group than that in control group. Ferrostatin-1, a ferroptosis inhibitor, could rescue the cell death induced by ART in U251 cells. Further examination of the mechanism revealed that the effect of ART on ferroptosis was partially governed by regulating iron homeostasis and p38 and ERK signaling pathway. These findings support that ART triggers ferroptosis in glioblastoma and might be a potential therapeutic agent for glioblastoma treatment.

Identification and functional analysis of novel oncogene DDX60L in pancreatic ductal adenocarcinoma.

BACKGROUND: Pancreatic ductal adenocarcinoma (PDAC) is a lethal cancer. Approximately 80% of patients initially diagnosed with locally advanced or metastatic disease survive only 4-11 months after diagnosis. Tremendous efforts have been made toward understanding the biology of PDAC. RESULTS: In this study, we first utilized next-generation sequencing technique and existing microarray datasets to identify significant differentially expressed genes between PDAC and non-tumor adjacent tissue. By comparing top significant survival genes in PDAC Gene Expression Profiling Interactive Analysis database and PDAC transcriptome data from patients, our integrated analysis discovered five potential central genes (i.e., MYEOV, KCNN4, FAM83A, S100A16, and DDX60L). Subsequently, we analyzed the cellular functions of the potential novel oncogenes MYEOV and DDX60L, which are highly expressed in PDAC cells. Notably, the knockdown of MYEOV and DDX60L significantly inhibited the metastasis of cancer cells and induced apoptosis. Further RNA sequencing analyses showed that massive signaling pathways, particularly the TNF signaling pathway and nuclear factor-kappa B (NF-κB) signaling pathway, were affected in siRNA-treated cancer cells. The siDDX60L and siMYEOV significantly inhibited the expression of chemokine CXCL2, which may potentially affect the tumor microenvironment in PDAC tissues. CONCLUSIONS: The present findings identified the novel oncogene DDX60L, which was highly expressed in PDAC. Transcriptome profiling through siRNA knockdown of DDX60L uncovered its functional roles in the PDAC in humans.

Temozolomide Drives Ferroptosis via a DMT1-Dependent Pathway in Glioblastoma Cells.

PURPOSE: Temozolomide is used in first-line treatment for glioblastoma. However, chemoresistance to temozolomide is common in glioma patients. In addition, mechanisms for the anti-tumor effects of temozolomide are largely unknown. Ferroptosis is a form of programmed cell death triggered by disturbed redox homeostasis, overloaded iron, and increased lipid peroxidation. The present study was performed to elucidate the involvement of ferroptosis in the anti-tumor mechanisms of temozolomide. MATERIALS AND METHODS: We utilized the CCK8 assay to evaluate cytotoxicity. Levels of lactate dehydrogenase (LDH), malondialdehyde (MDA), iron, and glutathione (GSH) were measured. Flow cytometry and fluorescence microscope were used to detect the production of reactive oxygen species (ROS). Western blotting, RT-PCR and siRNA transfection were used to investigate molecular mechanisms. RESULTS: Temozolomide increased the levels of LDH, MDA, and iron and reduced GSH levels in TG905 cells. Furthermore, we found that ROS levels and DMT1 expression were elevated in TG905 cells treated with temozolomide and were accompanied by a decrease in the expression of glutathione peroxidase 4, indicating an iron-dependent cell death, ferroptosis. Our results also showed that temozolomide-induced ferroptosis is associated with regulation of the Nrf2/HO-1 pathway. Conversely, DMT1 knockdown by siRNA evidently blocked temozolomide-induced ferroptosis in TG905 cells. CONCLUSION: Taken together, our findings indicate that temozolomide may suppress cell growth partly by inducing ferroptosis by targeting DMT1 expression in glioblastoma cells.

Characterization of Gas Absorption Modules Based on Flexible Mid-Infrared Hollow Waveguides.

A new gas absorption module, the substrate-embedded hollow waveguide (eHWG) model, is proposed. It consists of a substrate with a curved channel and a hollow waveguide. The hollow waveguide is curved into the channel and works as a gas absorption cell as well as a transmission medium for mid-infrared light. Owing to the low loss property of the hollow waveguide, the signal-to-noise ratio (SNR) was improved for the sensing system. A polycarbonate (PC) base tube was used to obtain flexibility in the fabrication of the hollow waveguide. A silver (Ag) layer and a silver iodide (AgI) layer were inner-coated to ensure a low loss property at the fingerprint wavelength of methane gas. A sensing system was established using a Fourier transform infrared spectrometer (FTIR), an external detector, and an eHWG. Experimental investigations were carried on the sensing performance of eHWGs with various channel shapes. Comparison studies were made on eHWGs embedded with Ag-coated or Ag- and AgI-coated hollow waveguides. The Ag- and AgI-coated hollow waveguides with inner diameters of 0.7, 1.4, and 2.0 mm were used in the eHWGs. The large bore waveguide had low loss but high bending additional loss. The large bore waveguide had a low detection limit due to high coupling efficiency with the light source. A limit of detection (LOD) as low as 2.7 ppm was attained for the system using the eHWG with the long and large bore waveguide.

Pharmacokinetics behaviors of l-menthol after inhalation and intravenous injection in rats and its inhibition effects on CYP450 enzymes in rat liver microsomes.

1. l-Menthol, as a kind of monocyclic terpene, is widely used in inhalation formulations, food and tobacco. The purpose of this study was to investigate the pharmacokinetic behavior of l-menthol as well as its influence on the activities of cytochrome P450 enzymes. 2. The pharmacokinetic behaviors of l-menthol after inhalation (50 mg/kg) and intravenous injection (10 mg/kg) were investigated. A rat liver microsomal model was adopted to elucidate the inhibitory effect of l-menthol on CYP1A2, CYP2C11, CYP2D1/2, CYP2D4, CYP2E1 and CYP3A1 using phenacetin, tolbutamide, omeprazole, dextromethorphan, chlorzoxazone and testosterone as probe drugs, respectively. 3. The plasma concentration reached the Cmax within 1.0 h (inhalation) and descended with the T1/2 of 8.53 and 6.69 h for inhalation and i.v. administration, respectively. IC50 for inhibition of l-menthol on CYP 450 enzymes were 4.35 µM for 2D4, 8.67 µM for 1A2, 13.02 µM for 3A1, 14.78 µM for 2D1/2, 234.9 µM for 2C11 and 525.4 µM for 2E1, respectively. 4. The results illustrate the pharmacokinetic process of l-menthol in rats and provide information for further rational applications. l-Menthol had moderate inhibitions on CYP2D4 and 1A2, which might affect the disposition of medicines primarily dependent on these pathways.

Metabolism and pharmacokinetics studies of allyl methyl disulfide in rats.

1. Allyl methyl disulfide (AMDS) is one of the main compounds in garlic, whereas its metabolism has not been studied yet. 2. In this work, we first identified the metabolites of AMDS in rat erythrocytes and rats using GC-MS. The transformation mechanism study among different metabolites was then conducted. The apparent kinetics of AMDS in rat erythrocytes and pharmacokinetics of AMDS by oral administration in rats were also studied. 3. The metabolic pathway study showed that AMDS was mainly metabolized in rats to allyl methyl sulfoxide (AMSO) and allyl methyl sulfone (AMSO2) through mechanisms of reduction, methylation and oxidation. The transformation mechanism study indicated that AMDS was firstly reduced to allyl mercaptan (AM) in rat erythrocytes, and then methylated to allyl methyl sulfide (AMS) by S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH), and finally oxidized to AMSO and AMSO2 by liver microsomes. The half-life of AMDS in rat erythrocytes was 6.285 ± 0.014 min while the half-lives of its active metabolites AMSO and AMSO2 in vivo were 18.17 and 17.50 h, respectively. Also, the large AUCs of the two active metabolites were observed, indicating potential applications of AMDS for certain pharmacological effects.

Nucleosides isolated from Ophiocordyceps sinensis inhibit cigarette smoke extract-induced inflammation via the SIRT1-nuclear factor-κB/p65 pathway in RAW264.7 macrophages and in COPD mice.

Background: Ophiocordyceps sinensis (C. sinensis) extracts have been found to have a therapeutic effect on patients with chronic obstructive pulmonary disease (COPD). Silent information regulator 1 (SIRT1) plays an important role in the regulation of inflammatory mediators and correlates with lung function and COPD exacerbations. The objective of this work was to explore the anti-inflammatory effect and preliminary pathways of nucleosides from cultured C. sinensis on RAW264.7 macrophages and COPD mice. Materials and methods: The nucleosides were extracted from cultured C. sinensis powder and further purified by macroporous resin D101 and glucan G10 columns. Inflammation and oxidative stress models in RAW264.7 macrophages and in mice were established by injection of cigarette smoke extract (CSE). We then examined how the isolated nucleosides regulated the production of the associated inflammatory mediators in vitro and in vivo by enzyme-linked immunosorbent assay, reverse transcription polymerase chain reaction, and Western blot. Results: The nucleosides inhibited inflammatory mediator expression of tumor necrosis factor-α, interleukin-6, interleukin-1ß, and nitric oxide in both the CSE-stimulated RAW264.7 macrophages and mice. Moreover, the nucleosides elevated SIRT1 activation and suppressed nuclear factor-κB (NF-κB)/p65 activation in vitro and in vivo. Nucleoside treatment significantly decreased the levels of the inflammatory mediators in the bronchoalveolar lavage fluid (BALF) and serum of the CSE-induced mice. The nucleosides also altered the recruitment of inflammatory cells in BALF and improved characteristic features of the lungs in the CSE-induced mice. Conclusion: These results show that the nucleosides suppressed COPD inflammation through the SIRT1-NF-κB/p65 pathway, suggesting that the nucleosides may be partly responsible for the therapeutic effects of cultured C. sinensis on COPD patients.

Methylallyl sulfone attenuates inflammation, oxidative stress and lung injury induced by cigarette smoke extract in mice and RAW264.7 cells.

In this study, we revealed that methylallyl sulfone (AMSO2), the metabolite of active organosulfur compounds, had anti-inflammatory and antioxidant effect in a cigarette smoke extract (CSE)-induced lung injury model. Firstly, histological analysis showed that the CSE group exhibited lung injury compared with the control, which was alleviated by AMSO2. Secondly, we estimated its anti-inflammatory capacity. The results indicated that pretreatment with AMSO2 significantly decreased CSE-elevated tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in serum. Thirdly, AMSO2 also showed antioxidant properties through enhancing activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) as well as reducing the level of malondialdehyde (MDA) and myeloperoxidase (MPO). Finally, we elucidated that AMSO2 alleviated inflammation and oxidative stress probably via suppressing ERK/p38 MAPK and inhibiting NF-κB expressions. In conclusion, we proposed that AMSO2 protected against the development of CSE-induced lung injury by reducing inflammatory cytokine levels and augmenting antioxidant activity via ERK/p38 MAPK and NF-κB pathways.

Protective effect of methylallyl sulfone in the development of cigarette smoke extract-induced apoptosis in rats and HFL-1 cells.

Although the organosulfur compounds from garlic have shown diverse pharmacological activities, the prototype drug was almost undetectable in vivo. As known, methylallyl sulfone (AMSO2) is the main metabolite of some active organosulfur compounds derived from garlic. The purpose of this article was to study the protective effect of AMSO2 on cigarette smoke extract (CSE) induced cell apoptosis in lungs in vivo and in vitro. The male rats were injected intraperitoneally with 900 µL of 100% CSE 3 times for three successive weeks. The rats from treatment groups were injected intraperitoneally with AMSO2 (50 mg/kg/day or 100 mg/kg/day) or DEX (1 mg/kg/day) for 21 days. We observed that pretreatment of AMSO2 effectively reversed apoptosis and oxidative stress in rats induced by CSE. Moreover, CSE-induced apoptosis in the HFL-1 cells was significantly suppressed by pretreated AMSO2 (400 µM) and DEX (0.1 mg/mL). Mechanistic studies suggested that this activity may arise from its effects on the regulation of p38 MAPK, Nrf-2 and Bcl-2/Bax signaling pathways. Overall, the metabolite of active organosulfur compounds AMSO2 might be a potential candidate for the treatment of CSE-induced apoptosis in rats.

Pharmacological Investigation of the Anti-Inflammation and Anti-Oxidation Activities of Diallyl Disulfide in a Rat Emphysema Model Induced by Cigarette Smoke Extract.

Diallyl disulfide (DADS) is the main organosulfur ingredient in garlic, with known antioxidant and anti-inflammatory activities. The aim of the present study was to investigate the effect of DADS on reducing the inflammation and redox imbalance in a rat emphysema model that was induced by intraperitoneal injection of cigarette smoke extract (CSE). Briefly, DADS exerted an anti-inflammation effect on emphysema rats through decreasing cell influx in the bronchoalveolar lavage fluid (BALF) and suppressing pro-inflammation cytokine production including tumor necrosis factor alpha (TNF-α), interleukin-1ß (IL-1ß), interleukin-6 (IL-6) via inhibiting the NF-κB pathway. In addition, levels of oxidative stress markers including malondialdehyde (MDA) and myeloperoxidase (MPO) were reduced, while the activities of glutathione (GSH), glutathione peroxidase (GSH-PX), superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) were markedly enhanced by DADS. Moreover, MMP-9 and TIMP-1 expression were down-regulated by DADS. Furthermore, the regulation effects of DADS on CD4⁺ and CD8⁺ T cells were observed. In conclusion, these encouraging findings suggest that DADS could be considered as a promising anti-inflammation and antioxidative agent for the treatment of emphysema.