**1. Introduction**

Diabetes mellitus (DM), a chronic metabolic disorder disease, is caused by the lack of insulin secretion (type Idiabetes mellitus) or insufficient insulin sensitivity (type IIdiabetes mellitus) [1,2], and the typical characteristic of the latter is post-prandial hyperglycemia. α-Glucosidase is a kind of membrane-bounded enzyme which is mainly found in intestinal epithelium cells and leads to the increase of blood glucose levels by hydrolyzing the glycosidic bonds of a polysaccharide [3–5]. As a result of that, α-Glucosidase inhibitors (AGIs), such as acarbose, miglitol and voglibose have become a widespread medical treatment in type IIdiabetes mellitus according to their glycemic control ability [6,7]. Nevertheless, existing AGIs often cause many side effects including abdominal pain, flatulence, diarrhea and other gastrointestinal disorders [8,9]. Hence, many natural medicine chemists were attracted to develop α-glucosidase inhibitors with lower toxicity and side effects for potential use. Some new α-glucosidase inhibitors have been researched like flavipesolides A–C [10], asperteretal E [11] and so on [12,13], and the discovery of better α-glucosidase inhibitors is still an urgen<sup>t</sup> need.

Marine fungi are proved to be rich sources of structurally unique and bioactive secondary metabolites. *Mycosphaerella* sp., which contributes the largest genus of Ascomycota, is a common plant pathogen widely distributed in terrestrial plant and marine environment [14–16]. As part of our ongoing investigation on new secondary metabolites from marine fungi in the South China Sea [17–21], a mangrove fungus, *Mycosphaerella* sp. SYSU-DZG01, collected from the fruit of the mangrove plant *Bruguiera*, Hainan Dongzhai Harbor Mangrove Reserve attracted

our attention because the EtOAc extract of the solid fermentation medium exhibited significant α-glucosidase inhibitory activity. Chemical investigation of the bioactive extract (Figure 1) lead to the discovery of four new metabolites, asperchalasine I (**1**), dibefurin B (**2**) and two epicoccine derivatives, (*R*)-9-((*R*)-10-hydroxyethyl)-7,9-dihydroisobenzofuran-1-ol (**3**), 2-methoxycarbonyl- 4,5,6- trihydroxy-3-methyl-benzaldehyde (**4**), together with seven known compounds, epicoccone B (**5**) [22], 1,3-dihydro-5-methoxy-7-methylisobenzofuran (**6**) [23], paeciloside A (**7**) [24], epicoccolide B (**8**) [25], asperchalasine A (**9**) [26], aspochalasin I (**10**) [27] and epicolactone (**11**) [28]. Their structures were established by extensive spectroscopic data and single-crystal X-ray diffraction analysis. Asperchalasine I possesses a distinct T-shaped skeleton containing one epicoccine moiety and one cytochalasan moiety. In bioactivity assays, compounds **1**, **8** and **9** exhibited α-glucosidase inhibitory activity and **1**, **4**, **6** and **8** showed antioxidant activity by scavenging DPPH·. Herein, the isolation, structure elucidation, α-glucosidase inhibitory and antioxidant activities of these compounds are reported.

**Figure 1.** Chemical structures of **1**–**11**.
