Day: November 22, 2022

Arsenic sulfide reverses cisplatin resistance in non-small cell lung cancer in vitro and in vivo through targeting PD-L1 was written by Tian, Wei;Sun, Yinping;Cheng, Yuping;Ma, Xiao;Du, Weina;Shi, Wenna;Guo, Qisen. And the article was included in Thoracic Cancer in 2021.Application of 63208-82-2 The following contents are mentioned in the article:

Background : Recent studies have found that programmed death ligand 1 (PD-L1) might be involved in chemotherapy resistance in non-small cell lung cancer (NSCLC). Arsenic sulfide (As₄S₄) has been recognized to have antitumor activities and enhance the cytotoxic effect of chemotherapy drugs. In this study, we aimed to verify the relationship between PD-L1 and cisplatin (DDP) resistance and identify whether As₄S₄ could reverse DDP resistance through targeting PD-L1 in NSCLC. Methods : The effect of As₄S₄ and DDP on cell proliferation and apoptosis was investigated in NSCLC cell lines. The expression of p53 and PD-L1 proteins was measured by western blotting anal. The levels of miR-34a-5p, miR-34a-3p and PD-L1 in cells were measured by real-time qPCR anal. Mouse xenograft models were established by inoculation with A549/DDP (DDP-resistant) cells. Results : Depletion of PD-L1 inhibited DDP resistance in A549/DDP and H1299/DDP cells. As₄S₄ was capable of sensitizing A549/DDP cells to DDP by enhancing apoptosis. As₄S₄ upregulated p53 expression and downregulated PD-L1 expression in A549/DDP cells. As₄S₄ increased miR-34a-5p level in A549/DDP cells. Inhibition of p53 by PFT-α partially restored the levels of PD-L1 and miR-34a-5p. Pretreatment with PFT-α suppressed the apoptosis rate induced by cotreatment of As₄S₄ and DDP in A549/DDP cells. Cotreatment of DDP and As₄S₄ notably reduced the tumor size when compared with DDP treatment alone in vivo. Conclusions : Upregulation of PD-L1 was correlated with DDP resistance in NSCLC cells. Mechanistic analyses indicated that As₄S₄ might sensitize NSCLC cells to DDP through targeting p53/miR-34a-5p/PD-L1 axis. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Application of 63208-82-2).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. Thiazoles frequently appear in peptide studies. Thiazoles can also be used as protected formyl groups, which can be released in later stages of complex natural product synthesis. Electrophilic attack at nitrogen depends on the presence of electron density at nitrogen as well as the position and nature of substituent linked to the thiazole ring.Application of 63208-82-2

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

Solid lipid nanocarriers embedded hydrogel for topical delivery of apremilast: In-vitro, ex-vivo, dermatopharmacokinetic and anti-psoriatic evaluation was written by Rapalli, Vamshi Krishna;Sharma, Swati;Roy, Aniruddha;Alexander, Amit;Singhvi, Gautam. And the article was included in Journal of Drug Delivery Science and Technology in 2021.COA of Formula: C20H18N2O2S The following contents are mentioned in the article:

The present work aimed to develop topical solid lipid nanocarriers (SLN) loaded hydrogel of apremilast (API) for psoriasis therapy to minimize the systemic adverse effects. The quality by design approach was implemented for the optimization of API loaded SLN using Box-Behnken design. SLN were prepared using hot emulsification followed by size reduction using probe sonication. The size and entrapment were found to be 167.70 nm ± 1.5 (0.238 PDI) and 63.84 ± 0.93%, resp. The FESEM images of SLN dispersion portrayed the spherical shape of nanocarriers. The in vitro drug release of SLN dispersion showed extended-release up to 18 h and followed the Korsmeyyar-Peppas model with a regression value of 0.958 (n = 0.330), and Akaike index criteria was 63.69. In vitro cell line study, the MTT assay depicted the formulation excipients had minimal effect, and high internalization was observed with SLN dispersion (1.4-fold). The Ct value reduction in the relative expression of TNF-α miRNA was 3-fold higher with SLN dispersion compared to the pos. control. The ex vivo skin retention and dermal distribution study by Coumarin-6 dye depicted an increase in permeation and retention with SLN formulation compared to free drug-loaded gel. The dermato-pharmacokinetic study of SLN formulation exhibited 2-fold higher drug retention in the epidermis and 5-fold higher in the dermis compared to free drug. This were stable for 3 mo without significant changes. The results suggest that API loaded SLN can be utilized for topical delivery for effective treatment of psoriasis by targeting skin layers. The API loaded SLN based topical gel formulation showed improved permeation, skin deposition and prolonged release compared to conventional preparation The designed preparation can signify a potential alternative for psoriasis treatment after clin. evaluation in near future. This study involved multiple reactions and reactants, such as 3-(Benzo[d]thiazol-2-yl)-7-(diethylamino)-2H-chromen-2-one (cas: 38215-36-0COA of Formula: C20H18N2O2S).

3-(Benzo[d]thiazol-2-yl)-7-(diethylamino)-2H-chromen-2-one (cas: 38215-36-0) belongs to thiazole derivatives. Thiazoles in peptides or their ability to bind proteins, DNA and RNA has led to many synthetic studies and new applications.Various laboratory methods exist for the organic synthesis of thiazoles. For example, 2,4-dimethylthiazole is synthesized from thioacetamide and chloroacetone.COA of Formula: C20H18N2O2S

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

The zebrafish antiapoptotic protein BIRC2 promotes Edwardsiella piscicida infection by inhibiting caspases and accumulating p53 in a p53 transcription-dependent and -independent manner was written by Cao, Lu;Yan, Dong;Xiao, Jun;Feng, Hao;Chang, Ming Xian. And the article was included in Frontiers in Immunology in 2021.COA of Formula: C16H19BrN2OS The following contents are mentioned in the article:

IAPs (inhibitors of apoptosis) are endogenous caspase inhibitors with multiple biol. activities. In the present study, we show functional characteristics of antiapoptotic protein BIRC2 (cIAP1) in response to Edwardsiella piscicida infection. Overexpression of BIRC2 in zebrafish larvae promoted the proliferation of E. piscicida, leading to a decreased larvae survival. The expression levels of caspases including casp3, casp8, and casp9 were significantly inhibited by BIRC2 overexpression in the case of E. piscicida infection. Treatment of zebrafish larvae microinjected with BIRC2 with the caspase activator PAC-1 completely blocked the neg. regulation of BIRC2 on the E. piscicida infection, with the reduced inhibition on the casp3 and without inhibition on casp8 and casp9. In contrast to the regulation of BIRC2 on the caspases, BIRC2 overexpression significantly induced the expression of p53, especially at 24 hpi. In addition to the cytoplasmic p53 expression, BIRC2 overexpression also induced the expression of the nuclear p53 protein. Further anal. demonstrated that BIRC2 could interact and colocalize with p53 in the cytoplasm. The numbers of E. piscicida in larvae overexpressed with BIRC2 and treated with pifithrin-μ (an inhibitor of mitochondrial p53) or pifithrin-α (an inhibitor of p53 transactivation) were lower than those of larvae without pifithrin-μ or pifithrin-α treatment. Critically, the p53 inactivators pifithrin-μ and pifithrin-α had no significant effect on larval survival, but completely rescued larval survival for zebrafish microinjected with BIRC2 in the case of E. piscicida infection. Collectively, the present study suggest that piscine BIRC2 is a neg. regulator for antibacterial immune response in response to the E. piscicida infection via inhibiting caspases, and accumulating p53 in a p53 transcription-dependent and -independent manner. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2COA of Formula: C16H19BrN2OS).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. The thiazole ring is notable as a component of the vitamin thiamine (B1). Electrophilic attack at nitrogen depends on the presence of electron density at nitrogen as well as the position and nature of substituent linked to the thiazole ring.COA of Formula: C16H19BrN2OS

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

Macrophage-biomimetic anti-inflammatory liposomes for homing and treating of aortic dissection was written by Liu, Jingxuan;Yang, Yueying;Liu, Xiao;Widjaya, Andy Samuel;Jiang, Baohong;Jiang, Yanyan. And the article was included in Journal of Controlled Release in 2021.Safety of 3-(Benzo[d]thiazol-2-yl)-7-(diethylamino)-2H-chromen-2-one The following contents are mentioned in the article:

Aortic dissection (AD) is a life-threatening disease featured by the dissection of intimal layer and the formation of a blood-filled false lumen within the aortic wall. Recent studies revealed that the formation and progression of AD lesions is closely related to vascular inflammation and macrophage infiltration. However, the potential efficacy of anti-inflammatory therapy on the prevention and treatment of AD has not been extensively investigated. Herein, we proposed a biomimetic anti-inflammatory liposome (PM/TN-CCLP) co-loaded with curcumin and celecoxib (CC), modified with cell-penetrating TAT-NBD fusion peptide (TN), and further camouflaged by isolated macrophage plasma membrane (PM), as a potential nanotherapy for AD. In vitro results showed that PM/TN-CCLP exhibited low cytotoxicity and elevated cellular uptake by inflammatory macrophages, and prominently inhibited the transendothelial migration, inflammatory responses and ROS generation of macrophages. Moreover, the PM/TN-CCLP treatment significantly prevented the H₂O₂-induced smooth muscle cell apoptosis. In vivo experiments were performed on the acute and chronic AD mouse models, resp. The results verified the elevated accumulation of PM-camouflaged liposome at the aorta lesions. Further, the anti-inflammatory liposomes, especially PM/TN-CCLP, could reduce the rupture rate of dissection, prevent the loss of elastic fibers, and reduce MMP-9 expression as well as macrophage infiltration in the aortic lesions. Notably, as compared with free drugs and TN-CCLP, the PM/TN-CCLP treatment displayed the longest survival period along with the minimal aortic injury on both acute and chronic AD mice. Taken together, the present study suggested that the macrophage-biomimetic anti-inflammatory nanotherapy would be a promising strategy for the prevention and therapy of aortic dissection. This study involved multiple reactions and reactants, such as 3-(Benzo[d]thiazol-2-yl)-7-(diethylamino)-2H-chromen-2-one (cas: 38215-36-0Safety of 3-(Benzo[d]thiazol-2-yl)-7-(diethylamino)-2H-chromen-2-one).

3-(Benzo[d]thiazol-2-yl)-7-(diethylamino)-2H-chromen-2-one (cas: 38215-36-0) belongs to thiazole derivatives. The thiazole ring has been identified as a central feature of numerous natural products, perhaps the most famous example of which is epothilone. There are numerous natural products that possess a thiazole ring with broad pharmacological activities. Thiamine, also known as vitamin B1, possesses a thiazole ring linked with 2-methylpyrimidine-4-amine as hydrochloride salt.Safety of 3-(Benzo[d]thiazol-2-yl)-7-(diethylamino)-2H-chromen-2-one

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

Spanning BODIPY fluorescence with self-assembled micellar clusters was written by Solomonov, Aleksei V.;Marfin, Yuriy S.;Tesler, Alexander B.;Merkushev, Dmitry A.;Bogatyreva, Elizaveta A.;Antina, Elena V.;Rumyantsev, Evgeniy V.;Shimanovich, Ulyana. And the article was included in Colloids and Surfaces, B: Biointerfaces in 2022.Synthetic Route of C20H18N2O2S The following contents are mentioned in the article:

BODIPY dyes possess favorable optical properties for a variety of applications including in vivo and in vitro diagnostics. However, their utilization might be limited by their water insolubility and incompatibility with chem. modifications, resulting in low aggregation stability. Here, we outline the route for addressing this issue. We have demonstrated two approaches, based on dye entrapment in micellar coordination clusters (MCCs); this provides a general solution for water solubility as well as aggregation stability of the seven BODIPY derivatives These derivatives have various bulky aromatic substituents in the 2,3,5,6- and meso-positions and can rotate relative to a dipyrrin core, which also provides mol. rotor properties. The mol. structural features and the presence of aromatic groups allows BODIPY dyes to be used as “supporting mols.”, thus promoting micelle-micelle interaction and micellar network stabilization. In the second approach, self-micellization, following BODIPY use, leads to MCC formation without the use of any mediators, including chelators and/or metal ions. In both approaches, BODIPY exhibits an excellent optical response, at a concentration beyond its solubilization limit in aqueous media and without undesired crystallization The suggested approaches represent systems used to encapsulate BODIPY in a capsule-based surfactant environment, enabling one to track the aggregation of BODIPY; these approaches represent an alternative system to study and apply BODIPY′s mol. rotor properties. The stabilized compounds, i.e., the BODIPY-loaded MCCs, provide a unique feature of permeability to hydrophilic ligand-switching proteins such as BSA; they exhibit a bright “turn-on” fluorescence signal within the clusters via macromol. complexation, thus expanding the possibilities of water-soluble BODIPY-loaded MCCs utilization for functional indicators. This study involved multiple reactions and reactants, such as 3-(Benzo[d]thiazol-2-yl)-7-(diethylamino)-2H-chromen-2-one (cas: 38215-36-0Synthetic Route of C20H18N2O2S).

3-(Benzo[d]thiazol-2-yl)-7-(diethylamino)-2H-chromen-2-one (cas: 38215-36-0) belongs to thiazole derivatives. Thiazole rings are planar and aromatic. Thiazoles are characterized by larger pi-electron delocalization than the corresponding oxazoles and have therefore greater aromaticity.Various laboratory methods exist for the organic synthesis of thiazoles. For example, 2,4-dimethylthiazole is synthesized from thioacetamide and chloroacetone.Synthetic Route of C20H18N2O2S

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

Dynamic regulation and requirement for ribosomal RNA transcription during mammalian development was written by Falcon, Karla T.;Watt, Kristin E. N.;Dash, Soma;Zhao, Ruonan;Sakai, Daisuke;Moore, Emma L.;Fitriasari, Sharien;Childers, Melissa;Sardiu, Mihaela E.;Swanson, Selene;Tsuchiya, Dai;Unruh, Jay;Bugarinovic, George;Li, Lin;Shiang, Rita;Achilleos, Annita;Dixon, Jill;Dixon, Michael J.;Trainor, Paul A.. And the article was included in Proceedings of the National Academy of Sciences of the United States of America in 2022.COA of Formula: C16H19BrN2OS The following contents are mentioned in the article:

RRNA (rRNA) transcription by RNA polymerase I (Pol I) is a critical rate-limiting step in ribosome biogenesis, which is essential for cell survival. Despite its global function, disruptions in ribosome biogenesis cause tissue-specific birth defects called ribosomopathies, which frequently affect craniofacial development. Here, we describe a cellular and mol. mechanism underlying the susceptibility of craniofacial development to disruptions in Pol I transcription. We show that Pol I subunits are highly expressed in the neuroepithelium and neural crest cells (NCCs), which generate most of the craniofacial skeleton. High expression of Pol I subunits sustains elevated rRNA transcription in NCC progenitors, which supports their high tissue-specific levels of protein translation, but also makes NCCs particularly sensitive to rRNA synthesis defects. Consistent with this model, NCC-specific deletion of Pol I subunits Polr1a, Polr1c, and associated factor Tcof1 in mice cell-autonomously diminishes rRNA synthesis, which leads to p53 protein accumulation, resulting in NCC apoptosis and craniofacial anomalies. Furthermore, compound mutations in Pol I subunits and associated factors specifically exacerbate the craniofacial anomalies characteristic of the ribosomopathies Treacher Collins syndrome and Acrofacial Dysostosis-Cincinnati type. Mechanistically, we demonstrate that diminished rRNA synthesis causes an imbalance between rRNA and ribosomal proteins. This leads to increased binding of ribosomal proteins Rpl5 and Rpl11 to Mdm2 and concomitantly diminished binding between Mdm2 and p53. Altogether, our results demonstrate a dynamic spatiotemporal requirement for rRNA transcription during mammalian cranial NCC development and corresponding tissue-specific threshold sensitivities to disruptions in rRNA transcription in the pathogenesis of congenital craniofacial disorders. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2COA of Formula: C16H19BrN2OS).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. The higher aromaticity of thiazole is due to delocalization of a lone pair of sulfur electrons across the ring, which is evidenced by chemical shifts of ring hydrogen at δ 7.27 and 8.77 ppm (C2 and C4), indicating diamagnetic ring current. Thiazole sulfonation occurs only under forcing conditions: the action of oleum at 250 °C for 3 hours in the presence of mercury(II) sulfate leads to 65% formation of 5-thiazole sulfonic acid.COA of Formula: C16H19BrN2OS

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

The effect of fluoxetine on astrocyte autophagy flux and injured mitochondria clearance in a mouse model of depression was written by Shu, Xiaodong;Sun, Yiming;Sun, Xiyang;Zhou, Yuanzhang;Bian, Yaqi;Shu, Zhaoma;Ding, Jianhua;Lu, Ming;Hu, Gang. And the article was included in Cell Death & Disease in 2019.HPLC of Formula: 63208-82-2 The following contents are mentioned in the article:

Although multiple hypotheses had been proposed to clarify the causes of depression, the accurate pathogenesis and effective treatment of depression still need to be solved. Pathol. change of astrocytes has been recognized to play a pivotal role in depression. Fluoxetine is the first selective serotonin reuptake inhibitor, however, the underlying mechanisms of fluoxetine are incompletely excavated. Emerging evidence shows that fluoxetine promotes autophagic processes in tumor cells. However, whether astrocytic autophagy gets involved in the cytoprotection of fluoxetine on astrocytes in depression treatment remains unexplored. Here we prepared chronic mild stress (CMS)-induced mouse model and treated mice with fluoxetine (10 mg/kg) for 4 wk to determine the correlation between proautophagic effect of fluoxetine and astrocyte protection in depression. Primary hippocampal astrocytes were cultured to investigate the potential mechanism of fluoxetine in regulating astrocyte autophagy. We found that fluoxetine (10 mg/kg) treatment promoted autophagosome formation and increased clearance of injured mitochondria, consequently protected astrocytes in CMS model mice. Fluoxetine (10μM) could also promote the autophagic flux unblocked via enhancing fusion of autophagosomes with lysosomes in primary astrocytes. Moreover, fluoxetine promoted mitophagy by increased colocalization of autophagosomes and mitochondria, eliminating damaged mitochondria in corticosterone-treated astrocytes. Further in vitro study showed that p53 presence is required for fluoxetine activated autophagy flux and fluoxetine promotes astrocytic autophagy in a p53-dependent mechanism. Collectively, this work gives us insights into a novel approach to treat depression depending on astrocytes, and provides a promising mol. target for the development of antidepressant drugs besides regulating neurotransmitters. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2HPLC of Formula: 63208-82-2).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. Thiazole is a five-membered, unsaturated, planar, π-excessive heteroaromatic containing one sulfur atom and one pyridine-type nitrogen atom at position 3 of the cyclic ring system. The nitrogen in thiazole is sp2 hybridized and the lone pair of electrons localized on the nitrogen is less reactive due to increased aromatic character and decreased basicity. It is protonated and alkylated/acylated at nitrogen forming hydrochloride and quaternary thiazolium salt.HPLC of Formula: 63208-82-2

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

Sorafenib-Loaded PLGA-TPGS Nanosystems Enhance Hepatocellular Carcinoma Therapy Through Reversing P-Glycoprotein-Mediated Multidrug Resistance was written by Tang, Maomao;Huang, Yuzhe;Liang, Xiao;Tao, Yaotian;He, Ning;Li, Zhenbao;Guo, Jian;Gui, Shuangying. And the article was included in AAPS PharmSciTech in 2022.HPLC of Formula: 38215-36-0 The following contents are mentioned in the article:

Multidrug resistance (MDR) is a key determinant for hepatocellular carcinoma chemotherapy failure. P-glycoprotein is one of the main causes of MDR by causing drug efflux in tumor cells. In order to solve this thorny problem, we prepared a sorafenib-loaded polylactic acid-glycolic acid (PLGA) – D-α-tocopheryl polyethylene glycol 1000 succinate (TPGS) nanoparticles (SPTNs). SPTNs were successfully synthesized through an ultrasonic emulsion solvent evaporation method with a favorable encapsulation efficiency of 90.35%. SPTNs were almost spherical in shape with uniform particle size (215.70 ± 0.36 nm), narrow polydispersity index (0.27 ± 0.02) and neg. surface charge (-26.01 ± 0.65 mV). In the cellular uptake assay, the intracellular coumarin-6 (C6) fluorescence of TPGS component-based PLGA nanoparticles (C6-PTNs) was 1.63-fold higher relative to that of PVA component-based PLGA nanoparticles (C6-PVNs). The half-maximal inhibitory concentration and apoptosis ratio of SPTNs against HepG2/MDR cells were 3.90 μM and 75.62%, resp., which were notably higher than free SF and sorafenib-PLGA-PVA nanoparticles (SPVNs). The anti-drug efflux activities of SPTNs were assessed by the intracellular trafficking assay using verapamil as a P-gp inhibitor. SPTNs could effectively inhibit the drug efflux in tumor cells detected by flow cytometry, and suppressed relative MDR1 gene as well as P-glycoprotein expression in tumor cells. Attributed to the MDR reversion effect of SPTNs, the in vivo antitumor efficacy experiment showed that SPTNs significantly inhibited the tumor growth of HepG2/MDR xenograft-bearing nude mice, and obviously reduced the toxicity against liver and kidney compared with SF treatment. In summary, SPTNs, as highly efficient and safe antitumor nano delivery systems, showed promising potential for hepatocellular carcinoma therapy through reversing P-glycoprotein-mediated MDR. This study involved multiple reactions and reactants, such as 3-(Benzo[d]thiazol-2-yl)-7-(diethylamino)-2H-chromen-2-one (cas: 38215-36-0HPLC of Formula: 38215-36-0).

3-(Benzo[d]thiazol-2-yl)-7-(diethylamino)-2H-chromen-2-one (cas: 38215-36-0) belongs to thiazole derivatives. Thiazoles frequently appear in peptide studies. Thiazoles can also be used as protected formyl groups, which can be released in later stages of complex natural product synthesis.Various laboratory methods exist for the organic synthesis of thiazoles. For example, 2,4-dimethylthiazole is synthesized from thioacetamide and chloroacetone.HPLC of Formula: 38215-36-0

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

Resveratrol inhibited the progression of human hepatocellular carcinoma by inducing autophagy via regulating p53 and the phosphoinositide 3-kinase/protein kinase B pathway was written by Zhang, Baichao;Yin, Xiaoning;Sui, Shaoguang. And the article was included in Oncology Reports in 2018.Reference of 63208-82-2 The following contents are mentioned in the article:

Resveratrol, a natural product, has been revealed to exert antitumor effects in multiple types of tumors. However, the antitumor effects of resveratrol on hepatocellular carcinoma (HCC) and its potential underlying mechanisms have not yet been elucidated. The present study demonstrated that resveratrol inhibited viability, proliferation, invasion and migration of HCC cells significantly in a time- and dose-dependent manner, indicating that resveratrol exerted antitumor effects in HCC. Furthermore, relative expression of autophagy-related proteins Beclin1 and LC3 II/I ratio was increased while p62 expression was decreased by resveratrol treatment dose-dependently. The LC3⁺ puncta formation, which represented autophagosome formation was also markedly dose-dependently upregulated by resveratrol treatment, suggesting that resveratrol induced autophagy in HCC cells. In addition, treatment with autophagy inhibitor 3-methyladenine (3-MA) counteracted the inhibitory effect of resveratrol on HCC cell proliferation, invasion and migration, indicating that suppressing autophagy may hamper the antitumor effect of resveratrol in HCC. It was revealed that resveratrol upregulated the expression of p53 while decreasing the ratio of phosphorylated protein kinase B (p-Akt)/Akt in HCC cells. Treatment with p53 inhibitor pifithrin-a and Akt activator insulin-like growth factor-1 decreased the expression of Beclin1 while significantly promoting cell proliferation, invasion and migration compared with the resveratrol treatment group. Taken together, the results of the present study revealed that resveratrol inhibited the proliferation and mobility of HCC cells through inducing autophagy via activating p53 and inhibiting phosphoinositide 3-kinase/Akt. Enhancing autophagy can augment the antitumor effects of resveratrol in HCC. Therefore, combining resveratrol with an autophagy inducer may be a viable option for treating HCC. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Reference of 63208-82-2).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. Thiazole rings are planar and aromatic. Thiazoles are characterized by larger pi-electron delocalization than the corresponding oxazoles and have therefore greater aromaticity. Electrophilic attack at nitrogen depends on the presence of electron density at nitrogen as well as the position and nature of substituent linked to the thiazole ring.Reference of 63208-82-2

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica

Interleukin-10 induces senescence of activated hepatic stellate cells via STAT3-p53 pathway to attenuate liver fibrosis was written by Huang, Yue-Hong;Chen, Ming-Hua;Guo, Qi-Lan;Chen, Zhi-Xin;Chen, Qing-Duo;Wang, Xiao-Zhong. And the article was included in Cellular Signalling in 2020.SDS of cas: 63208-82-2 The following contents are mentioned in the article:

Hepatic fibrosis is a wound healing process which results in deposition of excessive abnormal extracellular matrix (ECM) in response to various liver injuries. Activated hepatic stellate cells (HSCs) are the major sources of ECM and induction of senescence of activated HSCs is an attractive therapeutic strategy for liver fibrosis. Our previous studies have shown that interleukin-10 (IL-10) attenuates the carbon tetrachloride (CCL₄) – and porcine serum-induced liver fibrosis in rats. However, little is known about the mechanisms of IL-10 regulating the senescence of activated HSCs. The aim of this study is to uncover the underlying pathway by which IL-10 mediates activated HSCs senescence to attenuate liver fibrosis. In vivo, we found that IL-10 gene by hydrodynamics-based transfection attenuated CCL₄-induced liver fibrosis associated with senescence of activated HSCs in rats. In vitro experiment confirmed that IL-10 could induce senescence of activated HSCs via inhibiting cell proliferation, inducing cell cycle arrest, increasing the SA-β-Gal activity and enhancing expression of senescence marker protein p53 and p21. Treatment with Pifithrin-α, a specific inhibitor of p53, could abrogate IL-10-increased SA-β-Gal activity and expression of P53 and P21in activated HSCs. Lastly, IL-10 also increased the expression of total and phosphorylated signal transducers and activators of transcription 3(STAT3) and promoted phosphorylated STAT3 translocation from cytoplasm to nucleus. Treatment with cryptotanshinone, a specific inhibitor of STAT3, could inhibit the phosphorylation of STAT3 and its downstream proteins p53 and p21 expression and decrease the activity of SA-β-Gal in activated HSCs induced by IL-10. Taken together, IL-10 induced senescence of activated HSCs via STAT3-p53 pathway to attenuate liver fibrosis in rats and present study will provide a new mechanism of antifibrotic effects of IL-10. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2SDS of cas: 63208-82-2).

2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. Thiazole is a five-membered, unsaturated, planar, π-excessive heteroaromatic containing one sulfur atom and one pyridine-type nitrogen atom at position 3 of the cyclic ring system. The pyridine-type nitrogen in the thiazole ring deactivates the ring for electrophilic substitution reactions, which is further reduced in acid due to protonation of the thiazole ring.SDS of cas: 63208-82-2

Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica